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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
Cisatracurium
- ester hydrolysis and spontaneous nonenzymatic degredation (Hoffman) - NO histamine release
26
What prolongs NDMR duration?
- volatile anesthetics - antibiotics - age (extremes) - cardiovascular drugs - electrolyte imbalances - physiologic dysfunction
27
Which electrolyte mostly increases NDMR duration?
Increased Magnesium
28
What antibiotics mostly increase NDMR duration?
Aminoglycosides - Gentamycin - Tobramyclin Tetracycline Bacitracin
29
Reversal of NDMR
- binds to acetylcholinesterase receptor, blocking ACh - increases ACh at nicotinic and muscarinic receptors - must be given with anticholinergic (parasympatholytic)
30
Neostigmine for reversal
DOSE: 0.04-0.07MG/KG ONSET: 1-3m PEAK: 5-7m DURATION: 40-60m
31
Edrophonium for reversal
DOSE: 0.5-1 mg/kg PEAK: 1-5m DURATION: 5-20m
32
Atropine for reversal
DOSE: 15-70mcg/kg ONSET: 15-30 s PEAK: 2 m DURATION: 1-2 hrs
33
Glycopyrrolate for Reversal
DOSE: 10-20 mcg/kg ONSET: 1m PEAK: 5m DURATION: 2-4hrs
34
Sugammadex
reverses Rocuronium and Vecuronium - no anticholinergic necessary - no recurarisation - can reverse with no twitches? 16 mg/kg
35
What TOF ratio is needed for normal pharyngeal function?
0.9
36
Bradycardia observed after administration of succinylcholine to children is attributable to which mechanism
Muscarinic stimulation at the sinus node
37
What is the predominant mechanism for succinylcholine-induced tachycardia in adults?
Stimulation of nicotinic receptors at autonomic ganglia
38
Local anesthetics shift the balance of Na+ channels to _____
closed inactivated
39
Mechanism of action of local anesthetics
block the Na channel
40
What portion of the local anesthetic is responsible for the anesthetic action?
lipophilic portion
41
local anesthetics: | weak potency and short duration
procaine and chloroprocaine
42
local anesthetics: | moderate potency and intermediate duration
lidocaine, mepivicaine, and prilocaine
43
local anesthetics: | high potency and long duration
tetracaine, bupivicaine, ropivicaine, and etidocaine
44
Pharmacokinetics of local anesthetics
- 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
45
What cells extract amide local anesthetics through first pass?
endothelial
46
How does the pka affect local anesthetics?
onset
47
How does lipid solubility affect local anesthetics
anesthetic potency
48
How does protein binding affect local anesthetics
duration
49
How does tissue diffusibility affect local anesthetics
onset
50
How does vasodilator activity affect local anesthetics
potency and duration
51
Cm
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
the Cm of motor fibers is ____ that of sensory fibers
2x
53
Metabolism of amide local anesthetics
enzymes in the liver (slow) - slower metabolism leads to increased serum concentrations and potential for increased systemic toxicity
54
Metabolism of ester local anesthetics
hydrolysis in plasma
55
What metabolite may be responsible for ester allergic reactions?
para-aminobenzoic acid (PABA)
56
Alkalinization of local anesthetics
- increases the unionized franction of drug - more lipid soluble - speeds onset - enhances depth of block - increases spread of epidurals
57
How does epinephrine prolong LA duration?
vasoconstricts which decreases blood flow
58
What may reduce the risk of systemic toxicity in LA
decreasing rate of absorption
59
Lidocaine
- metabolized in liver - vasodilator - intrinsic analgesic properties
60
Mepivacaine
- similar to lidocaine | - lacks vasodilator activity
61
Bupivacaine
- renal excretion | - high affinity for heart muscle
62
Ropivacaine
- hepatic cytochrome P450 enzymes - less systemic toxicity - hepatic excretion
63
Prilocaine
- orthotoluidine converts hemoglobin to methemoglobin - cyanosis with decreases oxygen carrying capacity - methemoglobinemia can be reversed by methylene blue
64
Which *drug is a monoamine oxidase inhibitor associated with Serotonin syndrome?
Methylene Blue
65
MAOIs and which two classes of drugs can produce toxicity if mixed?
SRIs and Serotonin releasers
66
2 SNRIs
seratonin-norepinephrine reuptake inhibitor - effexor - cymbalta
67
Benzocaine
- weak acid (unionized) - ideal for topical anesthesia - rapid onset - methemoglobin possible
68
Cetacaine
may also cause methemoglobinemia
69
How does cocaine affect vessels?
vasoconstrictor
70
allergic reactions to LA
- esters > amides - preservatives - NO cross sensitivity
71
Risk factors for local anesthetic toxicity
- overdose - intravascular injection - injection into highly vascular tissue - decreased metabolism
72
Location of block and toxicity
Highest to Least - intercostal - caudal - epidural - brachial plexus - sciatic or femoral
73
How much local is administered in an intercostal block?
3-5 cc per level
74
Toxic plasma concentration of lidocaine/mepivicaine/prilocaine
5-10 mcg/mL
75
What 2 things may reduce seizure thresholds?
increased serotonin and CO2
76
Hypokalemia hyperpolarizes the cell and _____ seizure threshold
increases
77
Paradox of Local Anesthetics
Low concentrations block Na channels and prevent arrhythmias High concentrations eventually block automaticity and conduction
78
Why is Bupivicaine more likely than Lidocaine to bind to heart muscle?
largely unbound to protein
79
Large LA IV injection may cause:
- PVCs - wide QRS - V-tach - Asystole
80
LA Toxicity increases with:
- pregnancy - beta blockers - CCB - digitalis - epinephrine - phenylephrine - hypoxemia - acidosis - hypercarbia
81
Lipid Emulsion Therapy
- 1.5 mg/kg 20% lipid bolus | - 0.25 mg/kg/min infusion for at least 10 minutes
82
ACLS for LA
- limit epinephrine to 10-100mcg boluses - amiodarone preferred - vasopressin not recommended - avoid CCB and BB
83
If failure to respond to lipid emulsion and vasopressor therapy, begin ______
Cardiopulmonary Bypass
84
Transient Neurologic Syndrome (TNS)
- lower back and butt pain - 6-36 hours after spinal anesthesia - more common after lidocaine spinal
85
Cauda Equina Syndrome
diffuse injury across the lumbosacral plexus
86
Anterior Spinal Artery Syndrom
lower extremity weakness and paresis - more common in older patients - immediate imaging required
87
Max dosage of Lidocaine
4.5 mg/kg (7 mg/kg)
88
Max dosage of Mepivacaine
5 mg/kg (7 mg/kg)
89
Max dosage of Bupivacaine
2.5 mg/kg (3 mg/kg)
90
Max dosage of Tetracaine
1.5 mg/kg (2.5 mg/kg)
91
EMLA cream
Eutectic Mixture of Local Anesthetics - 2.5% Lidocaine and 2.5% prilocaine
92
1 amp (1cc) of 1:1000 in 10 cc =
1:10,000
93
1 amp of 1:1000 in 200cc
1:200,000
94
Spinal Anesthesia
- rapid in onset - gravity dependent - sensory and sympathetic block (2 level differential) [sensory farther down]
95
Epidural Anesthesia
- subarachnoid effect - diffuses into paravertebral area - test dose - continuous
96
COX2 inhibitor drug
Celecoxib (celebrex)
97
COX-1 vs COX-2
COX - (constitutive) COX-2 (inducible)
98
TXA2
platelet activation
99
PGI2 and PGE2
GI mucosa protection | Renal vasculature
100
PGE2 and PGD2
bronchodilation and renal function
101
PGH2
inflammation
102
COX-1 produces what?
Thromboxane A2 Prostacyclin Prostaglandin E2
103
COX-2 produces what?
proteases prostaglandins other inflammatory mediators
104
Aspirin and Platelets
aspirin binds permanently to platelets - blocks thromboxane - platelets must be replaced (7-14 days)
105
NSAIDS and renal function
- NSAIDS and COX-2 inhibitors reduce GFR - PGE2: peripheral edema - PGI2: hyperkalenia and acute renal failure
106
What is your enemy when taking care of a person using NSAIDS?
Hypovolemia - Check creatinine levels before giving Toradol - Normal 0.6-1.2
107
NSAIDS and PUD
- increase HCL secretion | - decrease mucin secretion
108
Which NSAID is the worse for GI?
Aspirin
109
Cardiovascular side effects of NSAIDS?
- heart failure - myocardial infarction - hypertension
110
Which NSAID is worse for the heart?
Celecoxib
111
NSAIDS and increased venous thromboembolus
COX2 inhibitrs result in decreased prostacyclins and unapposed thromboxane
112
AERD
Aspirin Exacerbated Respiratory Disease
113
Sampter's Triad
- aspirin sensitivity - nasal polyps - asthma
114
2 unlikely drugs that could cause Reye's syndrome
Alka Seltzer and Pepto-Bismol
115
Steven-Johnson Syndrome
hypersensitivty reaction, likely to Aspirin - toxic epidermal necrolysis
116
Leading cause of acute liver failure in the US
Acetaminophen overdose - co-toxic with ETOH
117
Capsaicin
decreases C-fiber activation in the presence of substance P
118
Clonidine
increases effect and duration of pain relief - centrally acting a2 agonist - hypotension

Quarter 3 (12 decks)

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