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Anesthesia based on Nebuchanedzzer II > Pharmacology pt 3 > Flashcards

Pharmacology pt 3 Flashcards

1
Q

______ has the shortest DOA of the BDZ

A

flumazenil

  • 0.7-1.3 hrs
  • concern for “recrudescence” of sedation from benzos
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2
Q

flumazenil MOA

A

benzodiazepine antagonist

- partial agonist

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3
Q 
Elimination half-life of:
Diazepam
Midazolam
Alprazolam
Lorazepam
Temazepam
Flumazenil
A 
Diazepam: 20-50 hrs
Midazolam: 2 hours
Alprazolam: 5-25 hours
Lorazepam: 10-20 hrs
Temazepam: 10 hrs

Flumazenil: 0.7-1.3 hrs

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4
Q

Desflurane degradation in the presence of desiccated carbon dioxide absorbent results in production of _____

A

carbon monoxide and heat

  • desflurane produces most CO
  • sevo produces most heat
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5
Q

Order of fluoride production for volatile anesthetics?

- theoretical risk of nephrotoxicity

A

Methoxyflurane&raquo_space; sevoflurane > isoflurane > desflurane

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6
Q

Compound A is produced from which volatile anesthetic?

A

Sevoflurane

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7
Q 
ED95 dose for:
Rocuronium
Cisatracurium
Vecuronium
Pancuronium
A

Rocuronium: 0.3
Cisatracurium: 0.04
Vecuronium: 0.04
Pancuronium: 0.06

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8
Q

Potency of neuromuscular blockers is best described by their ____

A

ED95

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9
Q

Effect of dexmedetomidine on BP over time

A

Biphasic response bc alpha 2 receptors are located in 2 diff places

  • initial dose: stimulates peripheral alpha-2 -> Inc in BP, decrease in HR and CO after 3 min
  • returns to baseline
  • Over the next hour: stimulates central alpha 2 -> reduce sympathetic tone, inc parasympathetic outflow -> slow decline in BP, inc in HR
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10
Q

MOA?
Onset of action ?
Duration of action?

  1. Cimetidine
  2. Ranitidine
  3. Famotidine
A

H2 receptor antagonist
- raises gastric pH

  1. Cimetidine (older):
    - 1-1.5 hrs
    - 3 hours
  2. Ranitidine:
    - 1 hrs
    - 9-10 hours
  3. Famotidine: 1 hrs
    - 1 hr
    - 10-12 hours
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11
Q

Which reversal agent is pulmonary edema seen in? (not muscle relaxant)

A

naloxone

- esp in large doses

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12
Q

CCBs to a naive pt will affect depolarizing and nondepolarizing NMBs how?

A

Mild augmentation to both
- CCBs prevent Ca2+ from crossing membrane -> less excitation-contraction

*CCBs to chronic users have very little effect

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13
Q

Why is meperidine falling out of favor?

A

Wide side effect profile and long half-life

*Libby Zion: the reason we have resident work hour limits

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14
Q

How does meperidine decrease shivering?

A

through the k opioid receptor (not mu)

*although it still affects mu

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15
Q

Major subtypes of opioid receptors

A

mu, kappa, delta

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16
Q

Actions of:
Mu1 receptor
Mu2 receptor

A

Mu1 receptor

  • analgesia
  • physical dependence

Mu2 receptor

  • respiratory depression
  • miosis
  • euphoria
  • dec GI motility
  • physical dependence
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17
Q

Actions of:
Kappa receptor
delta receptor

A

Kappa receptor

  • analgesia
  • dysphoria
  • sedation
  • miosis
  • inhibit ADH

delta receptor

  • analgesia
  • physical dependence
  • antidepressant
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18
Q

Nalbuphine MOA

A

Kappa agonist

Mu antagonist

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19
Q

What is morphine metabolized to? What is the active metabolite?

A

M3G and M6G

M6G is active metabolite

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20
Q

What is the only opioid that is also associated with inc in HR?

A

meperidine

- structurally similar to atropine

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21
Q

Liver blood flow dependent elimination is characteristic of _____ order kinetics

A

first

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22
Q

What is first order kinetics

A

drug elimination is proportional to drug concentration

- exponential

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23
Q

What is zero order kinetics?

A

enzymes involved in drug metabolism are at a max capacity

  • drug metabolism is INDEPENDENT of drug [ ] bx enzymes are saturated
  • rate of elimination of constant amt of medication is removed over time
  • linear
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24
Q

Drugs that follow zero-order kinetics
(- drug metabolism is INDEPENDENT of drug [ ] bx enzymes are saturated
- rate of elimination of constant amt of medication is removed over time)

A

THE PAW

Theophylline
Heparin
Ethanol
Phenytoin
ASA
Warfarin
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25
Q

Which induction agent works primarily by blocking glutamate?

A

Ketamine

  • NMDA receptor antagonist
  • NMDA r are a class of excitatory glutamate receptor
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26
Q

Which induction agent INDIRECTLY potentiates GABA receptors?

A

Ketamine

*etomidate, midaz, prop all potentiate via direct action

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27
Q

Succinylcholine effect on:
Upper esophageal sphincter tone
Intragastric pressure
Lower esophageal sphincter tone

A

Upper esophageal sphincter tone:
- decrease

Intragastric pressure
- increase

Lower esophageal sphincter tone
- increase (greater than intragastric pressure so NO inc risk of aspiration)

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28
Q

How does adding epi to LA work?

A

Prolongs duration of effect by decreasing local blood flow, LA stays in area of injection.
*does NOT change block onset time

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29
Q

is the active form of LA ionized (charged) or unionized (uncharged)?

A

ionized

*unionized pass through lipid membrane and reach targets easier than ionized molecules

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30
Q

The onset of action of LA is primarily a result of _____

A

lipid solubility
- pass thru membrane and reach site of action

pKa

  • aka ionization of drug
  • lower pKa = more unionized forms = faster onset (pass through lipid membrane and reach targets easier than ionized molecules)
  • higher pKa = more ionized forms = slower onset
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31
Q

Addition of what to LA speeds the onset of action?

A 
bicarb
- raises the pH of soln ->
more unionized fraction  ->
faster onset (pass through lipid membrane and reach targets easier than ionized molecules)

greater concentration
- ie. chloroprocaine pka 9 would predictably have slow onset, but actually

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32
Q

What is the MOA of ACEi?

A

catalyzes degradation of bradykinin ->
Arachidonic acid and nitric oxide

Inhibit the vasoconstrictive and sodium retentive properties of ATII (via aldosterone stim)

Promote the vasodilatory and natriuretic properties of bradykinin

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33
Q

____ cleaves angiotensinogen to angiotensin I

_____ then cleaves angiotensin I to angiotensin II

A

Renin

ACE

*ACEi block this conversion step

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34
Q

_____ release is the final step in the RAS pathway, which is stimulated by ___

A

Aldosterone
- promotes sodium and water retention in kidney via activation of Na-K pump in distal tubule

ATII

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35
Q

Cyclopentolate MOA and use?

A

Topical anticholinergic drug to induce mydriasis for ocular procedures

  • at risk for anticholinergic toxicity
  • dysarthria, tachycardia, psychosis, convulsions, disorientation
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36
Q

Acetylcholine effect on eyes

A

miosis

  • facilitates flow of aqueous humor
  • lowers IOP
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37
Q

Echothiophate MOA and use?

A

Anticholinesterase (inc ACh)
Treats refractory glaucoma by causing MIOSIS

*remember ACh effects on eyes:
miosis
- facilitates flow of aqueous humor
- lowers IOP

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38
Q

Timolol MOA and use

A

nonselective BB

glaucoma tx

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39
Q

Normally, the rate of rise of FA/FI is related to solubility or the blood:gas coefficient.
What explains why nitrous oxide has more rapid rise of FA/FI than desflurane

A

concentration effect

  • high [ ] anesthetic (ie. 70% nitrous oxide) increases rate of induction
  • nitrous oxide is the only gas that can demonstrate [ ] effect
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40
Q

What is the blood:gas coefficient for nitrous oxide and desflurane

A

Nitrous oxide: 0,47
Desflurane: 0.42

*the blood:gas coefficient is often the most important factor in rise of FA/FI, which is related to the speed of inhalational induction

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41
Q

*the________ is often the most important factor in rise of FA/FI, which is related to the speed of inhalational induction.
In order of most to least, what is the solubility of commonly used inhaled anesthetics

A

blood:gas coefficient

desflurane > nitrous oxide > sevoflurane > isoflurane

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42
Q

The _______ is a measure of lipophilicity. It is related to anesthetic potency and MAC

A

Oil:gas coefficient

  • higher the coefficient, the lower the MAC
  • ie: isoflurane has o:g of 99, and MAC of 1
  • desflurane has o:g of 19 and MAC of 6
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43
Q

What are the 4 potassium sparring diuretics?

A
  1. Spironolactone
  2. Triamterene
  3. Amiloride
  4. Eplerenone
    - block Na reab in collecting tubule, increasing K reab

*The K STAEs

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44
Q

Hyperkalemia sx on EKG other than peaked T waves

A
  1. shortened QT interval
  2. widening QRS
    3, PR prolongation
  • similar to hypermagnesemia
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45
Q

How much nalbuphine is useful to tx pruritus in neuraxial anesthesia?

A

5-10mg nalbuphine

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46
Q

What is mannitol?

A

A sugar alcohol that acts as an osmotic diuretic that is freely filtered at the glomerulus with poor reuptake back into the vasculature

*similar to hyperglycemia

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47
Q

What is Atrial Natriuretic peptide (ANP)?

A

released in response to atrial stretch (gen d/t volume overload)
- induces diuresis via natriuresis (not osmotic effect)

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48
Q

Prostaglandins affect fluid balance how?

A

They oppose ADH and RAAS

  • facilitates a diuretic and natriuretic effect
  • renal afferent arteriolar dilation
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49
Q

Mannitol is an osmotic diuretic, which pt population is it contraindicated in?

A

CHF - d.t initial increase in intravascular volume

  • use furosemide for diuresis in these pts instead
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50
Q

Terbutaline MOA

- causes (hyper/hypo)kalemia

A

beta2 agonist

- hypokalemia: temp intracellular shift

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51
Q

What is a phase 2 block?

A

occurs when succinylcholine remains on ACh receptors

  • keeps receptors activated and in OPEN position
  • occurs after prolonged admin of succinylcholine or single dose > 4mg/kg
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52
Q

Heparin has a 1:1 anti-Xa:IIa ratio.

What does LMWH have?

A

Increased anti-Xa:IIa ratio.

- shorter chain length does not inactivate thrombin to a significant degree, but it does inactivate Xa

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53
Q

LMWH is cleared (hepatically/renally)

A

renally,
- Smaller fragments of heparin in LMWH binds to macrophages in liver less -> cleared renally -> leading to longer plasma half lives and effective once daily regimen

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54
Q

Why is LMWH less likely to induce HIT?

A

smaller fragments of heparin in LMWH binds to platelets less

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55
Q

______ drugs prevent platelet activation and aggregation (clot prophylaxis)

_______ reduce fibrin formation (treatment of acute thrombi)

A

antiplatelet

Anticoagulant

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56
Q

4 Classes of antiplatelet drugs

- prevent platelet activation and aggregation (clot prophylaxis)

A
  1. Irreversible COX inhibitors
    - ASA
  2. ADP r inhibitors
    - Clopidogrel
    - Prasugrel
    - Ticlopidine
    - Ticagrelor
  3. PDE inhibitors
    - Cilostazol
    4, G IIb-IIIa inhibitors
    - abciximab
    - eptifibatide
    - tirofiban
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57
Q

5 Classes of anticoagulant drugs

- reduce fibrin formation (treatment of acute thrombi)

A
  1. Antithrombin III activators
    - Heparin
    - LMWH
  2. Heparin like factor Xa inhibitors
    - fondaparinux
  3. Direct factor Xa inhibitors
    - rivaroxaban
    - apixaban
  4. Direct thrombin inhibitors
    - bivalrudin
    - hirudin
    - argatroban
    - dabigatran
  5. Vit K antagonist
    - Warfarin
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58
Q

Which antiplatelet drug has the longest antiplatelet effect?

A

Ticlopidine (10-14 days)

  • ADP receptor inhibitor
  • drug works for several days after admin
  • impairs platelets for duration of its lifespan
  • needs to be stopped 2 weeks b4 surgery
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59
Q

Which anticoagulant drug has the longest effect?

A

warfarin/dabigatran

- 2-7 days

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60
Q

Phenytoin and Lidocaine are class Ib antiarrhythmic, that shortens which phase of the cardiac action potential?

A

Phase 0

- binds to VG sodium channels to terminate ventricular arrhythmias (in the past)

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61
Q

Drugs affecting Cardiac action potential:

- Class 1 (Na channel blocker, Phase 0)

A

1a: Quinidine, Procainamide
1b: Lidocaine, Phenytoin
1c: Flecainide, Propafenone

62
Q

Drugs affecting Cardiac action potential:

- Class 4 (Ca2+ channel blocker, Phase 2)

A
  1. Verapamil

2. Diltiazem

63
Q

Drugs affecting Cardiac action potential:

- Class 3 (K+ channel blocker, Phase 3)

A
  1. Amiodarone

2. Sotalol

64
Q

Drugs affecting Cardiac action potential:

- Class 2 (BB, phase 4)

A
  1. Propanolol

2. Metoprolol

65
Q

1a: Quinidine, Procainamide
1b: Lidocaine, Phenytoin
1c: Flecainide, Propafenone

What class blocker are these?
What do they block?
What phase of the cardiac action potential do they act on?
A

Class 1 (Na channel blocker, Phase 0 upstroke)

66
Q
  1. Verapamil
  2. Diltiazem
What class blocker are these?
What do they block?
What phase of the cardiac action potential do they act on?
A

Class 4 (Ca2+ channel blocker, Phase 2 plateau)

67
Q
  1. Amiodarone
  2. Sotalol
What class blocker are these?
What do they block?
What phase of the cardiac action potential do they act on?
A

Class 3 (K+ channel blocker, Phase 3 downstroke)

68
Q
  1. Propanolol
  2. Metoprolol
What class blocker are these?
What do they block?
What phase of the cardiac action potential do they act on?
A

Class 2 (BB, phase 4 flat bottom)

69
Q

Which NMB has the LEAST increase in dosage requirement for burn patients?

A

Mivacurium

- degraded by pseudocholinesterase (lvls are reduced in burn pts)

70
Q

Massive burn pts demonstrate resistance to which type of NMBs?

A

nondepolarizing NMB

Burn pts have MORE ACh receptors
- more receptors mean higher dose of free drug is required to compete with ACh

71
Q

Most NDMBs need to be increased by how much in burn pts to achieve same intubating conditions as healthy pts?

A

2-5x

72
Q

Why shouldnt you used norepi (a1, a2, b1 agonist) intramuscularly?

A

cause local ischemia and tissue necrosis

73
Q

Neostigmine effect on the eyes

A

Acetylcholinesterase inhibitor ->
Increases ACh available at motor end plate -> parasympathetic receptors in eye -> Miosis (pupillary constriction)

*NOT mydriasis

74
Q

Why is neostigmine (Acetylcholinesterase inhibitor) cotreated with glycopyrrolate?

A

muscarinic receptor antagonist

Counteracts side effects of neostigmine listed below:

  • Cardiac: bradycardia, hypotension
  • Pulm: bronchospasm, resp secretions
  • GI: peristalsis, inc GI secretions
  • Opth: miosis, decreased IOP
75
Q 
Blood:gas partition coefficients of:
Desflurane
Nitrous oxide
Sevoflurane
Isoflurane
Halothane
A 
Desflurane: 0.42
Nitrous oxide: 0.46
Sevoflurane: 0.69
Isoflurane: 1.46
Halothane: 2.54

*FA/FI will rise faster w/ agents with lower blood:gas partition coefficient (insoluble agents)

76
Q

How does the gas behave if the Blood:gas partition coefficient is >1? <1?

A

> 1: more drug is dissolved within blood

  • higher solubility
  • reduce rate of rise of FA/FI (slow induction)
  • ie. isoflurane (1.46), halothane (2.54)

<1: more drug exists in gaseous state than dissolved within blood
- lower solubility
- Inc rate of rise of FA/FI (fast induction)
- ie: Desflurane: 0.42
Nitrous oxide: 0.46
Sevoflurane: 0.69

77
Q

How do inhaled anesthetics affect spontaneous ventilation?

A

Minute ventilation will decrease

  • increase RR, but decreased TV
  • fast shallow breathing
78
Q

Why is metoclopramide contraindicated in pts with bowel obstruction?

A

Dopamine antagonist centrally
Cholinergic agonist peripherally

By promoting gastric emptying and increasing gastroesophageal sphincter tone, it decreases risk of pulmonary aspiration
- since it is a promotilitiy agent, you increase risk of bowel perf

79
Q

Etomidate (GABA agonist) can cause adrenal suppression by inhibiting the enzyme _______, even after a single dose

A

11-B-hydroxylase

- makes cortisol or aldosterone

80
Q

Etomidate effect on:
CMRO2
CBF
ICP

A

decreases all

81
Q

Anaphylaxis is a type ____ reaction and is ____ mediated

A

type 1

IgE mediated

82
Q

Hemolytic anemia is a type ____ reaction and is ____ mediated

A

Type II

Both IgG and IgM

83
Q

Contact dermatitis is a type ____ reaction and is ____ mediated

A

Type IV

T cell mediated

84
Q

Serum sickness is a type ____ reaction and is ____ mediated

A

Type III

immune complex mediated

85
Q 
At 1 MAC How does Isoflurane:
Affect BP?
HR?
Minute ventilation?
CVP?
A

BP: Lowers by decreasing SVR
Increases HR
Lower MV (Increases RR, reduces TV)
No change to CVP (too many complex factors at play)

86
Q

Tx for post op delirium d/t scopalamine?

A

Physostigmine

  • Acetylcholinesterase inhibitor
  • > prolongs presence of ACh in the synaptic cleft
  • can cross BBB and act as an antidote to antimuscarinic drugs (edrophonium and neostigmine cannot)

*Scope is a muscarinic antagonist (just like glycopyrrolate and atropine)

87
Q

*Scopolamine is a _______ (just like glycopyrrolate and atropine)

A

muscarinic antagonist

88
Q

Drug used to differentiate Myasthenia gravis from Lambert Eaton Myasthenic syndrome (LEMS)?

A

Edrophonium

  • acetylcholinesterase inhibitor
  • > prolongs presence of ACh in the synaptic cleft
  • reduce muscle weakness in pts with Myasthenia gravis (antibodies destroy ACh receptors)
89
Q

Physostigmine, Neostigmine, and Edrophonium MOA

- which one crosses the BBB?

A
  • acetylcholinesterase inhibitor
  • > prolongs presence of ACh in the synaptic cleft

*physostigmine

90
Q

Prophylaxis against nerve agent exposure?

A

Physostigmine

  • Acetylcholinesterase inhibitor
  • > prolongs presence of ACh in the synaptic cleft
  • can cross BBB and act as an antidote to antimuscarinic drugs (edrophonium and neostigmine cannot)

*also used as Tx for post op delirium d/t scopalamine

91
Q

Tx for gastroparesis. How?

A

Metoclopramide

    1. Accelerates gastric emptying
      1. Reduce gastric fluid volume
      2. Increased tone and amplitude of gastric contractions
      3. Enhance peristalsis of duodenum and jejunum
  • NO EFFECT on gastric pH
    • Dopamine antagonist at chemoreceptor trigger zone
  • Serotonin receptor antagonist at high doses
92
Q

MOA of Metoclopramide

A
  • Dopamine antagonist at chemoreceptor trigger zone

- Serotonin receptor antagonist at high doses

93
Q

Why should you avoid metoclopramide in pts with parkinsons disease?

A

Dopamine antagonist -> increases extrapyramidal symptoms

94
Q

Codeine is a prodrug that gets converted to what?

- What makes a poor metabolizer and an ultrarapid metabolizer?

A

Morphine via CYP2D6 ~ 10%

  • poor metabolizer: little CYP2D6, little analgesia from codeine
  • ultrarapid metabolizer: mult functional copies of CYP2D6 -> converts way more codeine to morphine -> accumulates quickly -> toxicity
95
Q

Why does Symptomatic hyponatremia decrease MAC?

A

CNS depression

96
Q 
How does this affect MAC?
Acute alcohol use
Chronic alcohol use
Acute meth/cocaine use
Chronic meth/cocaine use
A

Acute alcohol use: Decrease
Chronic alcohol use: Increase

Acute meth/cocaine use: Increase
Chronic meth/cocaine use: Decrease

97
Q

How does hypo/hyperthyroidism affect MAC?

A

It doesn’t
- unless there are alterations in temp

*Hypo/hypercapnia also doesnt

98
Q

Which metabolic derrangement does NOT affect MAC?

A

Metabolic alkalosis

*only severe metabolic acidosis affects MAC

99
Q

How are redheads (melanocortin-1 receptor gene) affected differently to meds?

A

Have HIGHER MAC requirements
More RESISTANT to lidocaine analgesia
More SENSITIVE to thermal pain

100
Q

How does Magnesium affect anesthetic requirement?

A

Volatile anesthetics: INCREASES MAC

TIVA: DECREASES MAC

101
Q

Why do infants increase volatile anesthetic uptake?

A

Lower FRC: less “air” to dilute volatile anesthetic

Higher minute ventilation: places more volatile anesthetic in alveoli

102
Q

MAC requirements peak at ___ age

A

6 months

103
Q

Cisatracurium

  • Intubating dose
  • Elim half life
A
  • Intubating dose: 0.1-0.15 mg/kg

- Elim half life: 25 min via hoffmann elimination

104
Q

What two things affect the reaction speed / metabolism of cisatracurium?

A

pH
Temp

*Last longer in pts with high temp and acidosis

105
Q

Defining feature of alfentanil?

A

Quick onset and offset of action
- d/t LOW pKa 6.5: primarily non-ionized at physiologic pH (~90%), moves across membranes rapidly -> fast onset and offset

*Generally, w/ opioids, the more lipid-soluble (higher partition coefficient), the faster the onset

106
Q

Partition coefficient of fentanyl vs morphine? Which one has faster onset?

A

Fentanyl: 813
Morphine: 1.4
- fentanyl is MUCH faster

  • The higher the partition coefficient, the earlier the onset of action
  • exception is alfentanil
107
Q

Which drugs cross membranes faster, ionized or non-ionized drugs?

A

Non-ionized, low pKa

- ie: alfentanil

108
Q

Which opioid is the most potent? WHy?

A

Sufentanil
- high affinity for opioid receptors
(fent and remi are 10x less potent)

109
Q

Which opioid has the shortest context sensitive half time?

A

Remifentanyl

  • d/t metabolism by nonspecific plasma esterases (red cell esterases)
  • just like esmolol

*not affected in pts with pseudocholinesterase deficiency

110
Q

Rule of “4” for alfentanil

A

Compared to fentanyl

  • 4x faster onset
  • 1/4 as potent
  • 1/4 shorter DOA
111
Q

Which drugs cause pain with injection? (5)

A
  1. Diazepam
  2. Etomidate
  3. Methohexital
  4. Propofol (bradykinin)
  5. Rocuronium
112
Q

Tramadol MOA

A

synthetic opioid analgesic w/ weak affinity for mu receptor, no affinity for delta or kappa receptors

  • PO most common
  • peak at 1-2 hours

Also is an SNRI: antinociceptive effect of descending inhibitory pathways of CNS

113
Q

Why is oral patiromer and sodium zirconium cyclosilicate good agents to use in an anuric pt with hyperkalemia?

A

oral K binder that elim K through the GI tract after
~ 7 hours for patiromer
~ 1 hour for sodium zirconium cyclosilicate

114
Q

What happens to PCWP initially after admin of Mannitol?

A

Increase in plasma volume -> Inc BP and CO -> Inc PCWP

- can cause pulmonary edema in pts with HF

115
Q

How does mannitol produce diuresis?

A

Increases osmotic pressure in proximal tubule and LOH ->
Decrease passive reabsorption of water ->
Increase RBF

116
Q

When mannitol is administered during neurologic and neurosurgical conditions, what is necessary for it to work?

A

Needs INTACT BBB

  • decreases cerebral edema and ICP
  • more effective at lowering water brain content than loops or hypertonic saline
117
Q

The only major contraindication for sugammadex is hypersensitivity to sugammadex, but what situations is it not recommended in?

A
  1. Pediatric pts
  2. Severe RF
  3. Reversal of anything other than Roc or Vec
  4. ICU use
118
Q

Sugammadex is physically incompatible with which drugs, and should not be administered with?

A
  1. Zofran
  2. Ranitidine
  3. Verapamil
119
Q

First sx of lidocaine toxicity?

A

numbness of lips/tongue

THEN visual/auditory disturbances

120
Q

Max recommended dose of Lidocaine with and without epi?

A

without epi: 5 mg/kg

with epi: 7 mg/kg

121
Q

How does renal failure affect the efficacy of NMBDs?

A

It doesn’t affect the efficacy, but it affects the clearance -> longer DOA
- Don’t need to dose adjust, but need to avoid long acting NMBDs (pancuronium) and intermediate NMBDs (vecuronium)

122
Q

How is rocuronium eliminated?

A

70% hepatic
10% renal
- Safe to use in pts with renal failure, with min extended DOA

123
Q

How is vecuronium eliminated?

A

Hepatibiliary system
but partially cleared in kidneys
- avoid in pts with RF

124
Q

Clinically significant effects of plasma cholinesterase (aka pseudocholinesterase aka butyrylcholinesterase), is seen when _____% of the enzyme activity is reduced

A

> 75%

125
Q

What is the normal dibucaine number?

Heterozygous atypical? Homozygous atypical?

A

Normal dibucaine number: 70-80
Heterozygous atypical: 50-60
Homozygous atypical: 20-30

*< 30 suggest prolonged paralysis
30-70 = variable

126
Q

Chloroprocaine MOA and metabolized how?

A

Ester LA

Hydrolysis by pseudocholinesterase

127
Q

Ester vs amide LA name difference?

A

Ester one “i”
- chloroprocaine

Amides more than 1 “i”.
- lidocaine, bupivacaine

128
Q

Mivacurium MOA

A

short acting NDMBs
- Hydrolysis by pseudocholinesterase

*just like chloroprocaine and succinylcholine

129
Q

Which drugs are metabolized by hydrolysis by pseudocholinesterase / plasmacholinesterase / butyrylcholinesterase?

A
  1. Succinylcholine
  2. Mivacurium
  3. Ester LA (2-chloro, tetracaine, procaine)
  4. cocaine
  5. Heroin
130
Q

Pts taking ectothiophate eye drops are at risk for what type of reaction with NMBDs?

A

Sig prolongation of succinylcholine up to 2 weeks after it is d/c

131
Q

Which muscle is MOST representative of abdominal muscle paralysis (diaphragm) and laryngeal muscle paralysis?

A

Corrugator supercilli muscle

  • moves eyebrows
  • MOST resistant to NMBs
  • first to recover
132
Q

Which muscle is MOST SENSITIVE to blockade?

A

Adductor pollicis muscle

  • good for emergence
  • recovery of fxn suggest greater recovery of muscles that are more resistant to blockade (diaphragm and laryngeal m)
133
Q

Recovery to TOF ratio > ___ at the adductor pollicis is recommended prior to extubation

A
  1. 9

- or else impairment of laryngeal m and diaphragm

134
Q

Where is the best place to monitor TOF for extubating conditions?

A

Adductor pollicis

- more sensitive

135
Q

Sustained eye opening, handgrip, tongue protrusion correlate with TOF ratio of ____

A

< 0.7

136
Q

Head lift, leg lift, tongue depressor, sustained hand grip correlate with TOF ratio of ____

A

0.7 - 0.9

137
Q

K-sparing diuretic mneumonic

A

The K+ STAys with ______
spironolactone, triamterene, amiloride

*Thiazides are assoc w/ hypokalemia

138
Q

Fenoldopam MOA

A

selective dopamine 1 agonist

  • Increases RBF despite SBP
  • NO alpha, beta, DA 2 receptor agonist activity
139
Q

Does nitroglycerin increase renal perfusion?

A

no, has selective vasodilatory effects on renal conductance

*Nitro is a veno-arterial dilator

140
Q

Does adenosine increase renal perfusion?

A

No, renal vasoconstriction, decrease renal perfusion

*adenosine is a vasodilator

141
Q

Ketamine effects on on CMRO2 and laryngeal reflexes?

A

Increase CMRO2

Preserved laryngeal reflexes

142
Q

Why is nitrous oxide associated with megaloblastic changes and agranulocytosis?

A

Decreased activity of Vit B12 dependent enzymes, methionine synthetase and thymidylate synthetase

143
Q

Why is methoxyflurane no longer used?

A

nephrotoxicity and hepatotoxicity

144
Q

Does aprepitant have QT prolongation?

Ciprofloxacin?

A

no

yes - cipro

145
Q

How does lithium affect NMBs?

How does it affect MAC?

A

Prolongs both nondepolarizing and depolarizing MR

  • reduces excitatory neurotransmission
  • reduces ACh release

Lowers MAC
- blocks brainstem release of NE, epi, dopamine

146
Q

______ is the only nondepolarizing NMB agent that is metabolized by pseudocholinesterase

A

Mivacurium

- prolonged by pseudocholinesterase def.

147
Q

LMWH more selectively inhibits ______ than UFH

A

activated factor X

148
Q

Direct thrombin inhibitors

A
  1. Argatroban
  2. Bivalrudin
  3. Lepirudin
  4. Desirudin
149
Q

Which abx potentiates NMB (prolonging paralysis)?

A

Aminoglycosides, clindamycin, tetracyclines

  • inhibits prejunctional ACh release
  • depress post junctional receptor sensitivity
150
Q

Does intrathecal morphine alter MAC?

Does IV lidocaine decrease MAC?

A

Nope

Yea

151
Q 
Glycopyrrolate effect on:
Gastric emptying
Gastric secretions
Upper esophageal sphincter tone
Lower esophageal sphincter tone
A

*decreases parasympathetic tone

Gastric emptying: delayed
Gastric secretions: decreased
Upper esophageal sphincter tone: lower
Lower esophageal sphincter tone: lower

152
Q

Which BP meds are contraindicated in pregnancy?

A

ACE-I

Anesthesia based on Nebuchanedzzer II (38 decks)

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