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
# 1/29/24 What are side effects of Dexamethasone (Decadron)?
Diabetic Risk of perioperative hyperglycemia Minimal side effects with 1 dose Perineal burning/itching ## Footnote slide 35
26
# 1/29/24 what is the dose for Dexamethasone (Decadron)
4mg/8mg/more? ## Footnote slide 35
27
# 1/29/24 what drug is a muscarinic antagonist and is a competitive antagonist of ACh?
Anticholinergics: Scopalamine Patch has central and peripheral effects ## Footnote slide 36
28
# 1/29/24 what is the peak concentration of the Scopalamine Patch?
Peak concentration 8-24 hours Apply 4 hours preop (onset) ## Footnote slide 36
29
# 1/29/24 what are the side effects of scopalamine patch?
dilated pupil/bright lights ## Footnote slide 36
30
# 1/29/24 What is the dose and priming dose for Scopolamine?
Dose: 1 patch for 24-72 hours on Post-Auricular Priming dose (140mcg) of 1.5 mg over next 72 hours. ## Footnote slide 36
31
What is the site comparison of Scopolamine?
## Footnote slide 37
32
What is the MOA if Bronchodilators (B-Receptor Agonists)?
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) ## Footnote slide 39
33
What is the delivery of inhaled SABA (Short Acting Beta Agonists)?
* 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** ## Footnote slide 40
34
What are side effects of SABA?
* TREMOR -B2 STIMULATION IN SKELETAL MUSCLE * TACHYCARDIA * TRANSIENT DECREASE IN ARTERIAL OXYGENATION * HYPERGLYCEMIA ## Footnote Slide 41
35
What are examples of SABA?
* Albuterol (Proventil) * Levo-Albuterol (Xopenex) ## Footnote slide 41
36
What are the effects of long term use of antacids if pH is too high?
* acid breakdown of food inhibited * acid rebound can occur ## Footnote slide 22
37
What are the effects of long term use of antacids with Magnesium based?
* common osmotic diarrhea * neurologic and neuromuscular impairment ## Footnote slide 22
38
What are the effects of long term use of antacids with Calcium based?
hypercalcemia ## Footnote slide 22
39
# ``` What are the effects of long term use of antacids with Sodium based?
Increased Sodium load -- rise for hypertensive patients ## Footnote slide 22
40
What is the MOA of Sodium Citrate (Bicitra)?
* Neutralizes Acid (BASE + ACID = SALT, CO2 AND WATER) * Protects *against **aspiration pneumonia*** (not aspiration) * increases intra-gastric volume ## Footnote slide 23
41
What is the effectiveness of Sodium Citrate (Bicitra)?
Works immediately but loses effectiveness in **30-60 minutes** ## Footnote slide 23
42
What is the dose of Sodium Citrate (Bicitra)?
15 - 30 mL PO ## Footnote slide 23
43
So what about a full stomach?
* give the H2 receptor antagonists (works pretty quickly) * avoid putting the to sleep * think of plan A, B, and C ## Footnote slide 24
44
What is the MOA of Dopamine Blockers?
Stimulates gastric motility (Prokinetic) - increases lower esophageal sphincter tone - stimulates peristalsis - relaxes pylorus and duodenum gastric emptying and intenstinal transit ## Footnote slide 25
45
What is the contraindication for Dopamine Blockers?
not administer to pateint with Dopamine depletion/ inhibition (Parkinson's) ## Footnote slide 25
46
What are the effects of Dopamine Blockers?
* 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 ## Footnote slide 25
47
What is the MOA of Metoclopramide (Reglan)?
FDA CLEARED DRUG FOR DIABETIC GASTROPARESIS ## Footnote slide 26
48
What are side effects of Metoclopramide (Reglan)?
* 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) ## Footnote slide 26
49
What is the dose of Metoclopramide (Reglan)?
10 - 20 mg IV over 3-5 minutes (15-30 mins prior to induction) ## Footnote slide 26
50
What is the MOA of Domperidone?
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 ## Footnote slide 27
51
What is the MOA of Droperidol (Inapsine)?
- 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 ## Footnote slide 28
52
What is the FDA 2001 Blackbox warning of Droperidol (Inapsine)?
* Prolonged QT intervals * Torsades with higher doses * lots of serious drug interactions: AMIODARONE, DIURETICS, SOTALOL, MINERALOCORTICOIDS, CALCIUM CHANNEL BLOCKERS ## Footnote slide 28
53
What is the dose of Droperidol (Inapsine)?
0.625-1.25 MG IV ## Footnote slide 28
54
What is MOA of Serotonin?
*RELEASED FROM CHROMAFFIN CELLS OF SMALL INTESTINE *STIMULATES VAGAL AFFERENTS THRU 5HT3 RECEPTORS *CAUSES VOMITING ## Footnote slide 30
55
Where can you find SEROTONIN (5-HT3) RECEPTORS?
UBIQUITOUS! * KIDNEY * COLON * LIVER * LUNG * STOMACH * HIGH CONCENTRATIONS IN BRAIN AND GI TRACT ## Footnote slide 31
56
H2 Receptor Antagonists are most commonly used in patients with what two diseases?
Duodenal Ulcer Disease and GERD
57
What affects do H2 Receptors antagonists have on gastric fluid?
Decrease Hypersecretion of gastric fluid Decrease Gastric fluid volume increase ph of gastric fluid
58
What are side effects of H2 receptor antagonists?
* Diarrhea * Headache * Skeletal muscle pain * Bradycardia * Elevated Creatinine
59
Prolong administration of H2 receptor antagonists can lead to overgrowth of what bacteria?
Candida Albicans
60
What is the relationship between increase use of H2 receptor antagonist and increased pulmonary infections?
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
Where enzyme is responsible for metabolizing Cimetidine (Tagamet) in the Liver?
CYP 450
62
What hormone does Cimetidine inhibit from binding to androgen receptors? What effects does this have on males?
Dihydrotestosterone Causes impotence and increased growth in breasts
63
What is the dose of Cimetidine?
150 – 300 mg administered IV; ½ the dose is administered for patients with renal impairment
64
Where is Ranitidine (Zantac) metabolized and where is it cleared?
Metabolized in the liver Cleared by the kidneys
65
What is the dose of Ranitidine (Zantac) and how is it administered?
50 mg Diluted in 20 cc and administered over 2 minutes ½ dose for patients with renal impairment
66
Does Famotidine (Pepcid) interfere with P450 enzymes?
No
67
What is the e ½ time of Famotidine (Pepcid)?
2.5 – 4 hrs
68
What drug interferes with phosphate absorption causing hypophosphatemia?
Famotidine
69
What is the dose of famotidine?
20 mg IV
70
What classification of medications irreversibly bind to acid secreting pumps and inhibit the movement of protons across gastric parietal cells?
Proton Pump Inhibitors
71
How many days does it take for Proton Pump Inhibitors (PPI) to begin to work?
Up to 5 day onset
72
PPI’s are more effective than H2 receptor antagonists in which disease processes?
* Healing esophagitis * healing ulcers * relieving symptoms of GERD * Treating Zollinger-Ellison syndrome * GI Hemorrhage
73
PPI’s block the enzyme that activates which anti-platelet medication?
Clopidogrel (Plavix)
74
List 4 common PPI’s
Omeprazole (Prilosec) Pantoprazole (Protonix) Lansoprazole (prevacid) Dexlansoprazole (dexilent)
75
Which PPI drug is administered orally in its Prodrug form?
Omeprazole (Prilosec)
76
Where does Omeprazole turn from its prodrug form to its active form?
It becomes active by protonating in the Parietal cells in the stomach
77
Acid- inhibition increases with repeated dosing of which PPI?
Omeprazole (Prilosec)
78
What is the dose of Omeprazole?
40 mg in 100cc
79
Over what time frame do you administer Omeprazole?
IV: 30 min PO: > 3hrs
80
What are the side effects of Omeprazole?
* Headache * agitation * confusion * abdominal pian * flatulence * N/V and Small bowel bacterial overgrowth
81
How long does it take Pantoprazole (Protonix) to decrease gastric volume and increase pH?
1 hour
82
Which drug has greater bioavailability and longer E1/2 time compared to Omeprazole (Prilosec)?
Pantoprazole (Protonix)
83
What is the dose and time of administration of Pantoprazole?
40 mg in 100 ml over 2-15 min
84
Aluminum and magnesium are used as a base in which type of antacids?
Particulate Antacids
85
Sodium, carbonate, citrate and bicarbonate are used as a base in which type of antacids?
Non-Particulate Antacids