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Quarter 3 > Anesthesia Final > Flashcards

Anesthesia Final Flashcards

1
Q

Reversal drugs for NDMR

A

anticholinesterases

  • inhibits AChase enzyme
  • leads to increases in Ach at NMJ to compete with NDMR
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2
Q

Common Twitch monitoring placements

A

Ulnar nerve
- abbductor pollicis

Facial Nerve (CN VII)

  • orbicularis occuli
  • corrugator supercili

Posterior Tibial nerve
- flexor hallucis brevis

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3
Q

Which muscle relaxant shows fade

A

non-depolarizing

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4
Q

Constant infusion of Succinylcholine

A

Neuromusclar response will quickly drop (stage I) and return to almost normal before going back down (stage II)

  • able to reverse with edrophonium in late stage II
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5
Q

Onset and duration of Succinylcholine

A

rapid onset (30-60s)

short duration (5-10 min)

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6
Q

Succinylcholine metabolism

A

Only a fraction reaches the NMJ

  • majority metabolized by pseudocholinesterase
  • rest diffuses away, limiting duration
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7
Q

how can you prolong the duration of Sux?

A

increase dose and decrease metabolism

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8
Q

What can decrease the amount of Pseduocholinesterases?

A

Pregnancy
Hypothermia
Liver disease
Drugs

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9
Q

What drugs decrease pseudocholinesterase?

A 
*Echothiphate eye drops
Organophosphate insecticide
cytotoxic drugs
MAO inhibitors
Anticholinesterases
Magnesium
Trimethaphan
Azathiprine
Ester anesthetics
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10
Q

Homozygous for abnormal pseudocholineserase enzyme

A

1/3000 patients

Will have a prolonged block
6-8 hours

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11
Q

Dibucaine

A

local anesthetic that inhibits pseudocholinesterase

  • Normal 80%
  • Homozygous 20%

Dibucaine Number (DN) is proportional to function (quality), not amount of enzyme

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12
Q

Side effects and complications of Succinylcholine

A
  • fasciculations
  • increased intracranial pressure
  • increase intragastric pressure
  • increased intraocular pressure
  • bradycardia and junctional arrhythmias
  • anaphylaxis
  • rhabdomyolysis
  • hyperkalemia
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13
Q

Succinylcholine and Dysrrhythmia

A

Muscarinic receptors in the sinus node

  • Bradycardia prone in children
  • more common after 2nd dose
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14
Q

Hyperkalemia and Succinylcholine

A

Burn Patient

  • OK in first 24 hours
  • should not use post-burn 1-2 years after

Trauma
- 1 week post event to 60 days

Upper Motor Neuron Injury

  • ok acutely
  • within 6 months of onset of symptoms
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15
Q

Amino-Steroid NDMR

A

pancuronium
rocuronium
vecuronium
pipecuronium

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16
Q

Benzylisoquinolone NDMR

A

atracurium and cisatracurium

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17
Q

NDMR agonist or antagonist?

A

competitive antagonist with ACh

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18
Q

Long acting NDMRs

A

Pancuronium
Doxacurium
Pipecuronium

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19
Q

Short acting NDMRs

A

Mivacurium

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20
Q

Pancuronium metabolism

A

renal clearance 80%

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21
Q

Mivacurium metabolism

A

plasma cholinesterase

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22
Q

Which 2 intermediate acting NDMRs are metabolized in the bile and hepatic?

A

Vecuronium and Rocuronium

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23
Q

Which intermediate acting NDMR releases histamine?

A

Atracurium

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24
Q

Atracurium

A
  • ester hydrolysis and spontaneous nonenzymatic degredation (Hoffman)
  • histamine release
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25
Q

Cisatracurium

A
  • ester hydrolysis and spontaneous nonenzymatic degredation (Hoffman)
  • NO histamine release
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26
Q

What prolongs NDMR duration?

A
  • volatile anesthetics
  • antibiotics
  • age (extremes)
  • cardiovascular drugs
  • electrolyte imbalances
  • physiologic dysfunction
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27
Q

Which electrolyte mostly increases NDMR duration?

A

Increased Magnesium

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28
Q

What antibiotics mostly increase NDMR duration?

A

Aminoglycosides

  • Gentamycin
  • Tobramyclin

Tetracycline
Bacitracin

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29
Q

Reversal of NDMR

A
  • binds to acetylcholinesterase receptor, blocking ACh
  • increases ACh at nicotinic and muscarinic receptors
  • must be given with anticholinergic (parasympatholytic)
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30
Q

Neostigmine for reversal

A

DOSE: 0.04-0.07MG/KG
ONSET: 1-3m
PEAK: 5-7m
DURATION: 40-60m

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31
Q

Edrophonium for reversal

A

DOSE: 0.5-1 mg/kg
PEAK: 1-5m
DURATION: 5-20m

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32
Q

Atropine for reversal

A

DOSE: 15-70mcg/kg
ONSET: 15-30 s
PEAK: 2 m
DURATION: 1-2 hrs

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33
Q

Glycopyrrolate for Reversal

A

DOSE: 10-20 mcg/kg
ONSET: 1m
PEAK: 5m
DURATION: 2-4hrs

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34
Q

Sugammadex

A

reverses Rocuronium and Vecuronium

  • no anticholinergic necessary
  • no recurarisation
  • can reverse with no twitches? 16 mg/kg
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35
Q

What TOF ratio is needed for normal pharyngeal function?

A

0.9

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36
Q

Bradycardia observed after administration of succinylcholine to children is attributable to which mechanism

A

Muscarinic stimulation at the sinus node

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37
Q

What is the predominant mechanism for succinylcholine-induced tachycardia in adults?

A

Stimulation of nicotinic receptors at autonomic ganglia

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38
Q

Local anesthetics shift the balance of Na+ channels to _____

A

closed inactivated

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39
Q

Mechanism of action of local anesthetics

A

block the Na channel

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40
Q

What portion of the local anesthetic is responsible for the anesthetic action?

A

lipophilic portion

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41
Q

local anesthetics:

weak potency and short duration

A

procaine and chloroprocaine

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42
Q

local anesthetics:

moderate potency and intermediate duration

A

lidocaine, mepivicaine, and prilocaine

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43
Q

local anesthetics:

high potency and long duration

A

tetracaine, bupivicaine, ropivicaine, and etidocaine

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44
Q

Pharmacokinetics of local anesthetics

A
  • weak bases (pKa > 7.4)
  • small amounts exist in lipid-soluble form
  • local anesthetics with pKs nearest to physiologic pH have the most rapid onset of action
  • vasodilator influences potency
  • increased blood flow increases absorption and decreases duration
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45
Q

What cells extract amide local anesthetics through first pass?

A

endothelial

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46
Q

How does the pka affect local anesthetics?

A

onset

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47
Q

How does lipid solubility affect local anesthetics

A

anesthetic potency

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48
Q

How does protein binding affect local anesthetics

49
Q

How does tissue diffusibility affect local anesthetics

50
Q

How does vasodilator activity affect local anesthetics

A

potency and duration

51
Q

Cm

A

minimum effective concentration of local anesthetic necessary to produce conduction blockade of nerve impulses

Influenced by:

  • nerve fiber diameter
  • increased pH
  • high frequency of nerve stimulation
52
Q

the Cm of motor fibers is ____ that of sensory fibers

53
Q

Metabolism of amide local anesthetics

A

enzymes in the liver
(slow)

  • slower metabolism leads to increased serum concentrations and potential for increased systemic toxicity
54
Q

Metabolism of ester local anesthetics

A

hydrolysis in plasma

55
Q

What metabolite may be responsible for ester allergic reactions?

A

para-aminobenzoic acid (PABA)

56
Q

Alkalinization of local anesthetics

A
  • increases the unionized franction of drug
  • more lipid soluble
    • speeds onset
    • enhances depth of block
    • increases spread of epidurals
57
Q

How does epinephrine prolong LA duration?

A

vasoconstricts which decreases blood flow

58
Q

What may reduce the risk of systemic toxicity in LA

A

decreasing rate of absorption

59
Q

Lidocaine

A
  • metabolized in liver
  • vasodilator
  • intrinsic analgesic properties
60
Q

Mepivacaine

A
  • similar to lidocaine

- lacks vasodilator activity

61
Q

Bupivacaine

A
  • renal excretion

- high affinity for heart muscle

62
Q

Ropivacaine

A
  • hepatic cytochrome P450 enzymes
  • less systemic toxicity
  • hepatic excretion
63
Q

Prilocaine

A
  • orthotoluidine converts hemoglobin to methemoglobin
  • cyanosis with decreases oxygen carrying capacity
  • methemoglobinemia can be reversed by methylene blue
64
Q

Which *drug is a monoamine oxidase inhibitor associated with Serotonin syndrome?

A

Methylene Blue

65
Q

MAOIs and which two classes of drugs can produce toxicity if mixed?

A

SRIs and Serotonin releasers

66
Q

2 SNRIs

A

seratonin-norepinephrine reuptake inhibitor

  • effexor
  • cymbalta
67
Q

Benzocaine

A
  • weak acid (unionized)
  • ideal for topical anesthesia
  • rapid onset
  • methemoglobin possible
68
Q

Cetacaine

A

may also cause methemoglobinemia

69
Q

How does cocaine affect vessels?

A

vasoconstrictor

70
Q

allergic reactions to LA

A
  • esters > amides
  • preservatives
  • NO cross sensitivity
71
Q

Risk factors for local anesthetic toxicity

A
  • overdose
  • intravascular injection
  • injection into highly vascular tissue
  • decreased metabolism
72
Q

Location of block and toxicity

A

Highest to Least

  • intercostal
  • caudal
  • epidural
  • brachial plexus
  • sciatic or femoral
73
Q

How much local is administered in an intercostal block?

A

3-5 cc per level

74
Q

Toxic plasma concentration of lidocaine/mepivicaine/prilocaine

A

5-10 mcg/mL

75
Q

What 2 things may reduce seizure thresholds?

A

increased serotonin and CO2

76
Q

Hypokalemia hyperpolarizes the cell and _____ seizure threshold

77
Q

Paradox of Local Anesthetics

A

Low concentrations block Na channels and prevent arrhythmias

High concentrations eventually block automaticity and conduction

78
Q

Why is Bupivicaine more likely than Lidocaine to bind to heart muscle?

A

largely unbound to protein

79
Q

Large LA IV injection may cause:

A
  • PVCs
  • wide QRS
  • V-tach
  • Asystole
80
Q

LA Toxicity increases with:

A
  • pregnancy
  • beta blockers
  • CCB
  • digitalis
  • epinephrine
  • phenylephrine
  • hypoxemia
  • acidosis
  • hypercarbia
81
Q

Lipid Emulsion Therapy

A
  • 1.5 mg/kg 20% lipid bolus

- 0.25 mg/kg/min infusion for at least 10 minutes

82
Q

ACLS for LA

A
  • limit epinephrine to 10-100mcg boluses
  • amiodarone preferred
  • vasopressin not recommended
  • avoid CCB and BB
83
Q

If failure to respond to lipid emulsion and vasopressor therapy, begin ______

A

Cardiopulmonary Bypass

84
Q

Transient Neurologic Syndrome (TNS)

A
  • lower back and butt pain
  • 6-36 hours after spinal anesthesia
  • more common after lidocaine spinal
85
Q

Cauda Equina Syndrome

A

diffuse injury across the lumbosacral plexus

86
Q

Anterior Spinal Artery Syndrom

A

lower extremity weakness and paresis

  • more common in older patients
  • immediate imaging required
87
Q

Max dosage of Lidocaine

A

4.5 mg/kg (7 mg/kg)

88
Q

Max dosage of Mepivacaine

A

5 mg/kg (7 mg/kg)

89
Q

Max dosage of Bupivacaine

A

2.5 mg/kg (3 mg/kg)

90
Q

Max dosage of Tetracaine

A

1.5 mg/kg (2.5 mg/kg)

91
Q

EMLA cream

A

Eutectic Mixture of Local Anesthetics

  • 2.5% Lidocaine and 2.5% prilocaine
92
Q

1 amp (1cc) of 1:1000 in 10 cc =

93
Q

1 amp of 1:1000 in 200cc

94
Q

Spinal Anesthesia

A
  • rapid in onset
  • gravity dependent
  • sensory and sympathetic block (2 level differential) [sensory farther down]
95
Q

Epidural Anesthesia

A
  • subarachnoid effect
  • diffuses into paravertebral area
  • test dose
  • continuous
96
Q

COX2 inhibitor drug

A

Celecoxib (celebrex)

97
Q

COX-1 vs COX-2

A

COX - (constitutive)

COX-2 (inducible)

98
Q

TXA2

A

platelet activation

99
Q

PGI2 and PGE2

A

GI mucosa protection

Renal vasculature

100
Q

PGE2 and PGD2

A

bronchodilation and renal function

101
Q

PGH2

A

inflammation

102
Q

COX-1 produces what?

A

Thromboxane A2
Prostacyclin
Prostaglandin E2

103
Q

COX-2 produces what?

A

proteases
prostaglandins
other inflammatory mediators

104
Q

Aspirin and Platelets

A

aspirin binds permanently to platelets

  • blocks thromboxane
  • platelets must be replaced (7-14 days)
105
Q

NSAIDS and renal function

A
  • NSAIDS and COX-2 inhibitors reduce GFR
    • PGE2: peripheral edema
    • PGI2: hyperkalenia and acute renal failure
106
Q

What is your enemy when taking care of a person using NSAIDS?

A

Hypovolemia

  • Check creatinine levels before giving Toradol
    • Normal 0.6-1.2
107
Q

NSAIDS and PUD

A
  • increase HCL secretion

- decrease mucin secretion

108
Q

Which NSAID is the worse for GI?

109
Q

Cardiovascular side effects of NSAIDS?

A
  • heart failure
  • myocardial infarction
  • hypertension
110
Q

Which NSAID is worse for the heart?

111
Q

NSAIDS and increased venous thromboembolus

A

COX2 inhibitrs result in decreased prostacyclins and unapposed thromboxane

112
Q

AERD

A

Aspirin Exacerbated Respiratory Disease

113
Q

Sampter’s Triad

A
  • aspirin sensitivity
  • nasal polyps
  • asthma
114
Q

2 unlikely drugs that could cause Reye’s syndrome

A

Alka Seltzer and Pepto-Bismol

115
Q

Steven-Johnson Syndrome

A

hypersensitivty reaction, likely to Aspirin

  • toxic epidermal necrolysis
116
Q

Leading cause of acute liver failure in the US

A

Acetaminophen overdose

  • co-toxic with ETOH
117
Q

Capsaicin

A

decreases C-fiber activation in the presence of substance P

118
Q

Clonidine

A

increases effect and duration of pain relief

  • centrally acting a2 agonist
  • hypotension

Quarter 3 (12 decks)

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