Cumulative Final (Exam 1) Flashcards

(74 cards)

1
Q

Describe the three depths of sedation?

A
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2
Q

What is the first inhaled anesthetic?

A
  • Diethyl ether
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3
Q

Describe the three depths of sedation?

A
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4
Q

What is the first inhaled anesthetic?

A
  • Diethyl ether
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5
Q

What are the disadvantages of using ether?

A
  • Flammable
  • Prolonged induction and emergence
  • Unpleasant odor
  • High incidence of nausea and vomiting
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6
Q

What is the anesthesia triad?

A

Amnesia, Analgesia, and Muscle Relaxation

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7
Q

How is amnesia acheived?

A

Stimulating inhibitory transmission or Inhibiting stimulatory transmissions via GABA and ACh

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8
Q

What is neuroplept anesthesia?

A

Using opioids, antipsychotics, and nitrous to induce anesthesia
Caused high incidence of awareness and dysphoria

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9
Q

What is stage I of anesthesia and the 3 planes?

A

Beginning of induction of anesthesia to loss of conciousness
* 1st plane: no amnesia or analgesia
* 2nd plane: amnestic but only partially analgesic (versed/fentanyl)
* 3rd plane: complete analgesia and amnesia

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10
Q

What is stage II of anesthesia?
What is this stage dangerous?

A

Loss of conciousness to onset of automatic breathing (ANS takes over)
* Eyelash reflex disappears
* Coughing, vomiting, and struggling may occur (risk of aspiration, bradycardia, and bronchospasm)
* Need to get through this stage as quickly as possible

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11
Q

What is stage 3 of anestheisa and the 4 planes?
What plane is desired prior to administering NMB?

A

Onset of automatic breathing to respiratory paralysis (surgical plane)
* 1st plane: automatic respiration to cessation of eyeball movements
* 2nd plane: cessation of eyeball movements to beginning of intercostal muscle paralysis; secretion of tears increases
* 3rd plane: beginning to completion of intercostal muscle paralysis; pupils dilate; desired plane prior to muscle paralysis (think 3 and 3)
* 4th plane: comple intercostal muscle paralysis to diphragmatic paralysis (apnea)

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12
Q

What is stage 4 of anesthesia?

A

Apnea until death… not desirable obviously

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13
Q

What is a partial and inverse agonist?
Examples of inverse agonists?

A
  • Partial: has less effect than full agonist even in higher doses
  • Inverse: binds at active site but causes an opposing effect from the agonist (propanolol, metoprolol, cetirizine, loratidine, prazosin, naloxone)
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14
Q

What is tachyphylaxis?
What 2 drugs undergo this?
What condition?

A

Tachyphylaxis: Rapid tolerance to a drug produce diminishing effects with each administration
- Albuterol (receptors downregulate due to repetition)
- Ephedrine (depletion of stored presynaptic catecholamines with each dose)
- Pheochromocytoma (decreased β receptors in response to catecholamines)

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15
Q

What drugs bind to intracellular receptors?

A
  • Insulin
  • Steroids
  • Milrinone
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16
Q

What is the vessel rich group?

A

Bolused drugs first distrubute to tissues that receive the bulk of arterial blood flow: the brain, heart, kidneys, and liver.

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17
Q

What is meant by a high and low VD?

A

High: drug distributes out of blood to tissue quickly - (lipid soluble drugs)
Low: drug stays within the cardiovascular system - (water soluble drugs)

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18
Q

What proteins do acidic and basic drugs bind to?

A

Acidic = Albumin
Basic = ⍺1-acid glycoprotein

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19
Q

If a drugs normal free fraction is 2% and their albumin is dropped by half, what is the new free fraction?
What does this mean?

A
  • 4%
  • This means with the same dose, the patient may have double the effect which usually comes with undesirable effects
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20
Q

What are the Phase I reactions?
What is their purpose?

A
  • Oxidation, Reduction, and Hydrolysis
  • Increases drug polarity to make them more water soluble in preparation for elimination
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21
Q

What is the phase II reaction?
What does it do?

A
  • Conjugation
  • Links covalently with a polar molecule to become more water soluble
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22
Q

What is flow limited clearance?

A
  • Rate of clearance is proportional to drug concentration
  • More hepatic flow = more clearance
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23
Q

What is capacity limited clearance?

A
  • Liver metabolism is the limiting factor for drug clearance
  • Only a certain amount can be cleared, regardless of changes in flow
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24
Q

If a drug has a 1/2 time of 10 minutes, what fraction of drug remains after 40 mins?

A

1/16 th

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25
What is context-sensitive half time? Why does this matter?
* The half time after a continuous infusion (assuming constant concentration) * Because many anesthetic drugs are lipid solubule and will accumulate in the tissues, meaning the longer the infusion is run, the longer the effects are seen.
26
What is the pneumonic to remember if a drug is ionized or not? What number are nonionized drugs?
* Weak **A**cids: pK **A**fter pH (pH - pK) * Weak **B**ases: pK **B**efore pH (pK - pH) * Negative numbers: “nicely negative numbers are nonionized”
27
What are some drugs we give that are weak acids and weak bases?
Weak acids: barbituates Weak bases: local anesthetics and opiods
28
What is ion trapping?
When a non-ionized drug becomes ionized in a part of the body and accumulates. Ex: Mother with normal pH and baby with acidic pH → local anesthetic/opiod becomes ionized in baby's body → ionized drug can't cross membranes and accumulates, causing a increased effect on the baby
29
How do you calculate therapeutic index?
LD50 ÷ ED50
30
What is the enatiomer of cisatracurium?
Atracurium
31
What drugs can decrease BIS?
Synergistic anesthetics like hypnotics, volatiles, NMB, opiods
32
What range of BIS prevents recall?
40-60
33
What should the EMG be on a paralyzed patient?
0
34
What is the supression ratio? What should it be?
- Measures how often the patient's BIS hit 0 - Should never have a number here or your anestheic is way too deep
35
How do sympathomimetics and sympatholytics affect the BIS?
- Sympathomimetics: may have a ↑ BIS due to ↑ catecholamines, but are still amnestic (ketamine) - Sympatholytics: BIS may be lower due to decreased SNS activity, despite having actually being more aware
36
What are the 5 effects of benzodiazepines?
1. Anxiolysis 2. Sedation 3. Anterograde amnesia (lasts longer than sedation) 4. Anticonvulsant 5. Spinal cord mediated muscle relaxation
37
What is the MOA of benzodiazepines?
- Binds to GABA A⍺/Ɣ subunits increasing Cl- entry into the cell causing hyperpolarization - Potentiates the GABA site
38
What are benzos different effects at ⍺1 and ⍺2 subunits?
- ⍺1: sedative, amnestic, anticonvulsant (most abundant) - ⍺2: anxiolytic, skeletal muscle
39
What are the pulmonary effects of midazolam?
- Dose dependent decrease in ventilation - Depresses swallowing reflex and upper airway activity = aspiration risk
40
What are the CV effects of midazolam?
↑ HR, ↓BP, ↓SVR CO unchanged
41
What is the preop dosing for midazolam for children and adults?
Children: 0.25-0.5mg/kg orally Adults: 1-5mg IV
42
What is the induction dose for midazolam?
0.1-0.2 mg/kg over 30 seconds
43
Why do valium and lorazepam burn on injection?
The solvent propylene glycol
44
What are the CNS effects of diazepam?
- ↓CBF/CMRO2 - Potent anticonvulsant - Can produce an isoelectric EEG
45
What is the induction dose for valium?
0.5-1.0 mg/kg IV
46
What drugs do flumazenil reverse?
Any drug that agonizes the GABA receptor - including psych and anti-seizure meds
47
What is the dosing for Romazicon?
0.2 mg IV then 0.1 mg q 1 min, up to 1 mg total
48
What 3 things does histamine release cause?
1. Contractions of airway smooth muscle 2. Gastric acid secretion 3. Release of NT in the CNS (ACh, norepinephrine, and serotonin)
49
What 4 drugs mentioned in lecture induce histamine release as a side effect?
- Morphine - Mivacurium (Mivacron) - Protamine - Atracurium (Tracrium)
50
What other receptors can histmaine activate at H1 and H2?
H1 - muscarinc, cholinergic, 5HT3, and ⍺-adrenergic H2 - 5HT3 and β1
51
What are the effects of histamine on the H1 receptor?
Inflammatory pain, hyperalgesia, and allergic rhino-conjunctivitis symptoms
52
What are the effects of histamine on the H2 receptor?
* ↑ cAMP (β1-like stimulation) * ↑ gastric acid and volume
53
What are the systemic effects from both H1 and H2 stimulation?
- Hypotension from NO release - Capillary permeability - Flushing - Prostacyclin release
54
Where are H1 receptors found?
* Vestibular system * Airway smooth muscle - Cardiac enodthelial cells
55
What are the 2 H1 antagonist given pre-op?
- Diphenhydramine (Benadryl) - Promethazine (Phenergan)
56
Why are second generation H1 antagonists sometimes preferred? Examples?
- Do not cross the BBB, less sedation - Cetirizine (Zyrtec) - Loratadine (Claritin)
57
Why is there a black box warning for promethazine (phenergan)?
- Fatal bronchospasms in children less than 2 - Causes tissue ischemia if infiltrated
58
What is the primary use for H2 antagonists
- Used for duodenal ulcer disease and GERD - Decreases hypersecretion of gastric fluid - ↓ Gastric volume, ↑ pH
59
What are the 3 examples of H2 receptor antagonists?
Cimetidine (Tagamet) Rantidine (Zantac) Famotidine (Pepcid)
60
Which H2 antagonist would you avoid in patients with bone disorders?
Famotidine - interferes with phosphate absorption causing hypophosphatemia
61
What is the MOA of PPIs?
Inhibits movement of protons in gastric parietal cells - only works on currently active pumps
62
What are the time considerations for PPI's?
Can take up to 5 days to have onset Not much effectiveness in same day cases
63
What is the naming convention for PPIs?
-prazole
64
What are PPIs most effective for?
Decreasing gastric volume and controlling acidity
65
Which PPI can begin to start working as soon as 1 hour?
Pantoprazole, although probably not effective enough to prevent aspiration prior to surgery
66
What type of antacid would we never give pre-op? Why?
Particulate (aluminum/magnesium based) Would be worse if aspirated
67
Which patients do we always give sodium citrate (Bicitra)?
C sections
68
Why do we give Bicitra to surgical patients?
It works immediately to neutralize stomach acid to protect against aspiration pneumonitis
69
What is the MOA for dopamine blockers?
Stimulate gastric motility by increasing lower esophageal sphincter tone and relaxing pylorus and duodenum. | Dopamine inhibts muscle movement
70
What is the naming convention for 5HT3 antagonists?
-setron
71
What is the most important side effect to know about ondansetron (Zofran)?
Causes slight QT prolongation
72
What are the preposed MOA of anti-emetic effects of corticosteroids?
Controls endorphin release and produces anti-inflammatory effects (less pain, less opioids)
73
When should you administer decadron to prevent PONV? Airway edema?
* PONV: 2 hours before extubating (takes 2 hours for onset) * Airway: immediately after intubation
74
Why is scopolamine the anticholinergic of choice for prevention of PONV?
Produces more desirable effects than the others: