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Adv Anes. Pharm Spring 2024 > Exam 1/Lecture 4: "other" preoperative medication > Flashcards

Exam 1/Lecture 4: "other" preoperative medication Flashcards

1
Q

Lecture 1/29/24

What are the 2 cells that produce histamine ?

A

basophils
mast cell

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2
Q

Lecture 1/29/24

What are 3 characteristics of histamines that benefits the body

A
  • Contraction of smooth muscles in airways
  • Secretion of acid in the stomach
  • Release of neurotransmitters in the CNS

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3
Q

Lecture 1/29/24

What are the 3 neurotransmitters in the CNS that are release by histamines?

A

Acetylcholine
nor-epi
serotonin

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4
Q

Lecture 1/29/24

What are the 4 drugs that induced histmaine release?

A
  • Morphine
  • Mivacurium (mivacron)
  • Protamine
  • Atracurium (tracrium)

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5
Q

Lecture 1/129/24

H1 and H2 receptor can be found in which cholinergic and adrenergic system and what is the reaction to histamine?

A
  • H1
    muscarinic, cholinergic, 5-HT3 and a-adrenergic
    Hyperalgesia and inflammatory pain (insect stings)
    Allergic rhino-conjunctivitis symptoms
  • H2
    5-HT3, and B-1
    Elevates camp (B1-like stimulation)
    Increases acid/volume production

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6
Q

Lecture 1/29/24

What type of agonists is an antihisamine?
Is an antihisamine reversible or irreversible?

A

inverse agonist
reversible

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7
Q

Lecture 1/29/24

What are some symptoms that a CRNA could see if the patient H1 and H2 is activated ?

5 symptoms were stated in lecture

A
  • Hypotension (release of nitric oxide)
  • Capillary permeability
  • Flushing
  • Prostacyclin release
  • Tachycardia

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8
Q

Lecture 1/29/24

Where are H1 receptors found in the body?

3 areas were stated in lecture

A

vestibular system
airway smooth muscle
cardiac endothelial cells

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9
Q

Lecture 1/29/24

What are 3 effective benefits from taking a H1 receptor antagonist?

A
  • Effective for motion sickness for ambulatory patients
  • Possible protection against bronchospasm
  • Provides some cardiac stability (indicated in anaphylaxis)

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10
Q

Lecture 1/29/24

What are the side effects of a H1 receptor antagonists?

A
  • Blurred vision
  • Urinary retention
  • Dry mouth
  • Drowsiness (1st generation)

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11
Q

Lecture 1/29/24

What are examples of H1 receptor anatgonist?

A
  • diphenhydramine (Benadryl)
  • Promethazine (Phenergan)
  • Cetirizine (Zyrtec)
  • Loratadine (Claritin)

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12
Q

Lecture 1/29/24

Which H1 receptor antagonist can be use as an antipruritic , may inhibit afferent arc of oculo-emetic reflex and stimulates ventilation?

A

Diphenhydramine (Benadryl)

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13
Q

Lecture 1/29/24

What is the elimination 1/2 time and dosing of Diphenhydramine (Benadryl)?

A
  • elimination 1/2 time = 7-12 hours
  • dosing = 25 -50 mg IV

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14
Q

Lecture 1/29/24

What is the elimination 1/2 time and dosing of Promethazine (Phenergan)?

A

elimination 1/2 time = 9- 16 hours
* dosing = 12.5 - 25mg IV
onset 5 minutes

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15
Q

Lecture 1/29/25

Which H1 receptor antagonists is an anti- emetic, used as a rescue drug, and can be used to reduce peripheral pain levels?

A

Promethazine (Phenergan)?

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16
Q

What are the 2 black box wrongs that were issued in 2005 and 2009 for Promethazine (Phenergan)?

A
  • Resp. arrest to children under 2
  • infiltration in the tissue can casue necrosis

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17
Q

Lecture 1/29/24

What are the beneifts of takning a H2 receptor anatgonist?

3 benefits were stated during lecture

A
  • Decrease hypersection of gastric fluid (H+)
  • Decrease gastric volume
  • Increase pH

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18
Q

Lecture 1/29/24

What class of medication is most commonly used in duodenal ulcer disease /GERD

A

H2 Receptor anatagonts

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19
Q

1/29/24

ondansetron does not hit which receptors?

A

No dopamine, histamine, adrenergic, or cholinergic activity
No CNS effects

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20
Q

1/29/24

what are the side effects of Ondansetron?

A

Studies equivocal with droperidol, dexamethasone, metoclopramide
Side effects: HA, diarrhea
Slight QT prolongation

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21
Q

1/29/24

what is the plasma 1/2 life and dose of Ondansetron?

A

1/2 life: 4 hours
dose 4-8 mg IV

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22
Q

1/29/24

what is it MOA of Corticosteroids?

A
  • centrally inhibit prostaglandin synthesis and control endorphin release
    -Increase effectiveness for 5HT3 antagonists and droperidol
    -Anti-inflammatory…less postop pain…less opioid

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23
Q

1/29/24

what is an example of corticosteroids?

A

Dexamethasone (Decadron)

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24
Q

1/29/24

what is the onset of Dexamethasone (Decadron)?

A

Delay in onset of 2 hours
Efficacy persists for 24 hours

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25
Q

1/29/24

What are side effects of Dexamethasone (Decadron)?

A

Diabetic Risk of perioperative hyperglycemia
Minimal side effects with 1 dose

Perineal burning/itching

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26
Q

1/29/24

what is the dose for Dexamethasone (Decadron)

A

4mg/8mg/more?

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27
Q

1/29/24

what drug is a muscarinic antagonist and is a competitive antagonist of ACh?

A

Anticholinergics: Scopalamine Patch

has central and peripheral effects

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28
Q

1/29/24

what is the peak concentration of the Scopalamine Patch?

A

Peak concentration 8-24 hours
Apply 4 hours preop (onset)

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29
Q

1/29/24

what are the side effects of scopalamine patch?

A

dilated pupil/bright lights

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30
Q

1/29/24

What is the dose and priming dose for Scopolamine?

A

Dose: 1 patch for 24-72 hours on Post-Auricular

Priming dose (140mcg) of 1.5 mg over next 72 hours.

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31
Q

What is the site comparison of Scopolamine?

A

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32
Q

What is the MOA if Bronchodilators (B-Receptor Agonists)?

A

STRUCTURE SIMILAR TO EPINEPHRINE

STIMULATORY G PROTEINS STIMULATORY G PROTEINS
*ACTIVATE CAMP
*DECREASE CA+2 ENTRY
*DECREASE CONTRACTILE PROTEIN SENSITIVITY TO CA+2

MOA:
*REDUCE INFLAMMATORY CELL ACTIVATION
*DIRECTLY RELAX SMOOTH MUSCLE….15% INCREASE FEV1, 6 MINUTES (2 PUFFS)

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33
Q

What is the delivery of inhaled SABA (Short Acting Beta Agonists)?

A
  • DISCHARGE INHALER WHILE TAKING A SLOW DEEP BREATH OVER 5-6 SECONDS
  • HOLD BREATH AT MAX INSPIRATION FOR 5-6 SECONDS
  • APPROXIMATELY 12% OF DRUG REACHES LUNGS
  • ETT DECREASES BY 50-70% (MECHANICAL VENTILATION INCREASES D/T POSITIVE PRESSURE)

*REPEATED Q 4HRS

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34
Q

What are side effects of SABA?

A
  • TREMOR
    -B2 STIMULATION IN SKELETAL MUSCLE
  • TACHYCARDIA
  • TRANSIENT DECREASE IN ARTERIAL OXYGENATION
  • HYPERGLYCEMIA

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35
Q

What are examples of SABA?

A
  • Albuterol (Proventil)
  • Levo-Albuterol (Xopenex)

slide 41

36
Q

What are the effects of long term use of antacids if pH is too high?

A
  • acid breakdown of food inhibited
  • acid rebound can occur

slide 22

37
Q

What are the effects of long term use of antacids with Magnesium based?

A
  • common osmotic diarrhea
  • neurologic and neuromuscular impairment

slide 22

38
Q

What are the effects of long term use of antacids with Calcium based?

A

hypercalcemia

slide 22

39
Q

```

What are the effects of long term use of antacids with Sodium based?

A

Increased Sodium load – rise for hypertensive patients

slide 22

40
Q

What is the MOA of Sodium Citrate (Bicitra)?

A
  • Neutralizes Acid (BASE + ACID = SALT, CO2 AND WATER)
  • Protects against aspiration pneumonia (not aspiration)
  • increases intra-gastric volume

slide 23

41
Q

What is the effectiveness of
Sodium Citrate (Bicitra)?

A

Works immediately but loses effectiveness in 30-60 minutes

slide 23

42
Q

What is the dose of
Sodium Citrate (Bicitra)?

A

15 - 30 mL PO

slide 23

43
Q

So what about a full stomach?

A
  • give the H2 receptor antagonists (works pretty quickly)
  • avoid putting the to sleep
  • think of plan A, B, and C

slide 24

44
Q

What is the MOA of Dopamine Blockers?

A

Stimulates gastric motility (Prokinetic)
- increases lower esophageal sphincter tone
- stimulates peristalsis
- relaxes pylorus and duodenum
gastric emptying and intenstinal transit

slide 25

45
Q

What is the contraindication for Dopamine Blockers?

A

not administer to pateint with Dopamine depletion/ inhibition

(Parkinson’s)

slide 25

46
Q

What are the effects of Dopamine Blockers?

A
  • EXTRAPYRAMIDAL REACTIONS (EASILY CROSSES BBB)
  • ORTHOSTATIC HYPOTENSION
  • SOME EFFECTS ON CHEMORECEPTOR TRIGGER ZONE
    ESP CINV AND S/P CSECTION BUT < 5-HT3 DRUGS
  • NO CHANGE IN GASTRIC PH

slide 25

47
Q

What is the MOA of
Metoclopramide (Reglan)?

A

FDA CLEARED DRUG FOR DIABETIC GASTROPARESIS

slide 26

48
Q

What are side effects of
Metoclopramide (Reglan)?

A
  • ABDOMINAL CRAMPING (IF RAPID IV)
  • MUSCLE SPASMS
  • HYPOTENSION
  • SEDATION
  • INCREASES PROLACTIN RELEASE
  • NEUROLEPTIC MALIGNANT SYNDROME (HIGH TEMP, MUSCLE RIGIDITY, TACHYCARDIA, CONFUSION)
  • DECREASES PLASMA CHOLINESTERASE LEVELS (SLOWS METABOLISM OF SUCCINYLCHOLINE, MIVACURIUM, ESTER LA)

slide 26

49
Q

What is the dose of
Metoclopramide (Reglan)?

A

10 - 20 mg IV over 3-5 minutes
(15-30 mins prior to induction)

slide 26

50
Q

What is the MOA of Domperidone?

A

Different than Metoclopramide:
* not cross BBB
* no anticholinergic activity

Increases Prolactin secretion by Pituitary to a greater degree

No FDA approval
* dysrhythmias
* sudden death
* available out of the country

slide 27

51
Q

What is the MOA of
Droperidol (Inapsine)?

A
  • Developed for Schizophrenia and Psychosis
  • Strong D2 Antagonist:
  • Extrapyramidal symptoms
  • Neuroleptic Malignant Syndrome
  • Avoid other CNS depressants –Barbituates, Opioids, General Anesthetics
  • More effective than Metoclopramide (Reglan)
  • Equally effective to 4 mg Ondansetron
  • much cheaper

slide 28

52
Q

What is the FDA 2001 Blackbox warning of Droperidol (Inapsine)?

A
  • Prolonged QT intervals
  • Torsades with higher doses
  • lots of serious drug interactions: AMIODARONE,
    DIURETICS, SOTALOL, MINERALOCORTICOIDS, CALCIUM CHANNEL BLOCKERS

slide 28

53
Q

What is the dose of Droperidol (Inapsine)?

A

0.625-1.25 MG IV

slide 28

54
Q

What is MOA of Serotonin?

A

*RELEASED FROM CHROMAFFIN CELLS OF SMALL INTESTINE

*STIMULATES VAGAL AFFERENTS THRU 5HT3 RECEPTORS

*CAUSES VOMITING

slide 30

55
Q

Where can you find
SEROTONIN (5-HT3) RECEPTORS?

A

UBIQUITOUS!

  • KIDNEY
  • COLON
  • LIVER
  • LUNG
  • STOMACH
  • HIGH CONCENTRATIONS IN BRAIN AND GI TRACT

slide 31

56
Q

H2 Receptor Antagonists are most commonly used in patients with what two diseases?

A

Duodenal Ulcer Disease and GERD

57
Q

What affects do H2 Receptors antagonists have on gastric fluid?

A

Decrease Hypersecretion of gastric fluid

Decrease Gastric fluid volume

increase ph of gastric fluid

58
Q

What are side effects of H2 receptor antagonists?

A
  • Diarrhea
  • Headache
  • Skeletal muscle pain
  • Bradycardia
  • Elevated Creatinine
59
Q

Prolong administration of H2 receptor antagonists can lead to overgrowth of what bacteria?

A

Candida Albicans

60
Q

What is the relationship between increase use of H2 receptor antagonist and increased pulmonary infections?

A

Increase use changes the acidic environment allowing yeast and bacteria to grow. Pulmonary infections increase if gastric fluid with high bacterial growth is aspirated

61
Q

Where enzyme is responsible for metabolizing Cimetidine (Tagamet) in the Liver?

62
Q

What hormone does Cimetidine inhibit from binding to androgen receptors? What effects does this have on males?

A

Dihydrotestosterone

Causes impotence and increased growth in breasts

63
Q

What is the dose of Cimetidine?

A

150 – 300 mg administered IV; ½ the dose is administered for patients with renal impairment

64
Q

Where is Ranitidine (Zantac) metabolized and where is it cleared?

A

Metabolized in the liver

Cleared by the kidneys

65
Q

What is the dose of Ranitidine (Zantac) and how is it administered?

A

50 mg

Diluted in 20 cc and administered over 2 minutes

½ dose for patients with renal impairment

66
Q

Does Famotidine (Pepcid) interfere with P450 enzymes?

67
Q

What is the e ½ time of Famotidine (Pepcid)?

A

2.5 – 4 hrs

68
Q

What drug interferes with phosphate absorption causing hypophosphatemia?

A

Famotidine

69
Q

What is the dose of famotidine?

70
Q

What classification of medications irreversibly bind to acid secreting pumps and inhibit the movement of protons across gastric parietal cells?

A

Proton Pump Inhibitors

71
Q

How many days does it take for Proton Pump Inhibitors (PPI) to begin to work?

A

Up to 5 day onset

72
Q

PPI’s are more effective than H2 receptor antagonists in which disease processes?

A
  • Healing esophagitis
  • healing ulcers
  • relieving symptoms of GERD
  • Treating Zollinger-Ellison syndrome
  • GI Hemorrhage
73
Q

PPI’s block the enzyme that activates which anti-platelet medication?

A

Clopidogrel (Plavix)

74
Q

List 4 common PPI’s

A

Omeprazole (Prilosec)

Pantoprazole (Protonix)

Lansoprazole (prevacid)
Dexlansoprazole (dexilent)

75
Q

Which PPI drug is administered orally in its Prodrug form?

A

Omeprazole (Prilosec)

76
Q

Where does Omeprazole turn from its prodrug form to its active form?

A

It becomes active by protonating in the Parietal cells in the stomach

77
Q

Acid- inhibition increases with repeated dosing of which PPI?

A

Omeprazole (Prilosec)

78
Q

What is the dose of Omeprazole?

A

40 mg in 100cc

79
Q

Over what time frame do you administer Omeprazole?

A

IV: 30 min
PO: > 3hrs

80
Q

What are the side effects of Omeprazole?

A
  • Headache
  • agitation
  • confusion
  • abdominal pian
  • flatulence
  • N/V and Small bowel bacterial overgrowth
81
Q

How long does it take Pantoprazole (Protonix) to decrease gastric volume and increase pH?

82
Q

Which drug has greater bioavailability and longer E1/2 time compared to Omeprazole (Prilosec)?

A

Pantoprazole (Protonix)

83
Q

What is the dose and time of administration of Pantoprazole?

A

40 mg in 100 ml over 2-15 min

84
Q

Aluminum and magnesium are used as a base in which type of antacids?

A

Particulate Antacids

85
Q

Sodium, carbonate, citrate and bicarbonate are used as a base in which type of antacids?

A

Non-Particulate Antacids

Adv Anes. Pharm Spring 2024 (7 decks)

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