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MTSA Orientation Test 2 > Regional Lecture Test > Flashcards

Regional Lecture Test Flashcards

0
Q

What reverses a local anesthetic?

A

Time

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1
Q

What are the three characteristic segments all local anesthetics have?

A
  • intermediate carbon group (ester/amide)
  • unsaturated ring system
  • amine end
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2
Q

What is the most prominent problem of local anesthetics?

A

inadvertent vascular injection

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3
Q

What is responsible for the classification of a local anesthetic and why?

A
  • The ester or amide linkage

- the only difference between the aromatic ring and amine end

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4
Q

How can you differentiate between an ester and amide by looking at the name?

A
  • Esters have one i (procaine,cocaine)

- Amides have two i’s (lidocaine, mepivacaine)

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5
Q

What does lipid solubility relate to?

A

High lipid solubility is proportional to potency of a local anesthetic

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6
Q

Definition of Lipophilic/Hydrophobic

A

Lipophilic-fat loving

Hydrophobic-water fearing

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7
Q

Why does lipid solubility affect potency?

A

Nerve sheath covering is lipid based so other lipids pass through easily

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8
Q

What type of binding is related to the duration of action?

A

Protein Binding

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9
Q

Between duration of action and potency, which is more related to lipid solubility?

A

Potency

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10
Q

Sodium channels have what three functional states?

A

Resting (closed)
Inactive
Open

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11
Q

What are the two parts to a local anethestic?

A

Nonionized (fat soluble

Ionized (water soluble)

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12
Q

How does LA work? Part 1

A
  • -Once injected LA dissociates into its active(non-charged) and inactive(charged) forms
  • -the non-charged(lipid soluble) part passes through the lipid soluble membrane
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13
Q

How does LA work? Part 2

A
  • -the lipid portion that passes through, binds with minerals in axoplasm
  • -the reassociated LA blocks the action potential by blocking Na pump and prevents the pain stimulus from moving down the nerve
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14
Q

What is the definition of pKa?

A

pKa is the pH at which 50% of the drug is in the charged (ionized, inactive) form and the remaining half is the uncharged (active) state

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15
Q

What is the correlation of pKa and potency?

A

–the lower the pKa the greater the potency

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16
Q

How does pKa work?

A
  • -the lower the pH of the environment the drug is placed into compared to it pKa, the more ionized (inactive) it becomes
  • -so the higher the pKa the more inactive it becomes
  • -the lower the pKa the more active drug left to work
17
Q

Why are vasoconstrictors added to LA’s?

A

To decrease the spread , vascular uptake of the drug

18
Q

What 4 helpful things happen when adding a vasoconstrictor to the LA?

A
  • higher local concentration of the LA
  • longer duration of effect
  • reduced systemic absorption
  • hemostasis for improved visualization
19
Q

When should we not use a vasoconstrictor?

A
  • fingers
  • toes
  • nose
  • hose
20
Q

What drug reverses the negative results of a vasoconstrictor in a given area?

A

-phentolamine 1.5-5mg

21
Q

How are LA with epi packaged?

A

Red top with red lettering on label

22
Q

What does adding NaHCO3 do to the LA?

A
  • stored at pH of 4-6 for shelf life (decreases unionized/active form)
  • buffering with NaHCO3 increases the unionized/active form to increase speed of penetration to nerve tissue
23
Q

All LA, except which three, produce vascular smooth muscle relaxation?

A
  • Cocaine (topical)
  • Ropivacaine (parenteral)
  • Lidocaine (parenteral)
24
Q

If VSM relaxation occurs, it increases the risk of ________?

A

toxic effects

25
Q

Which type of tissue receives the most amount of LA if it enters blood stream and why?

A

Muscle because it is highly perfused

26
Q

How are esters metabolized?

A
  • Ester hydrolysis occurs through esterase
  • Occurs in plasma, RBC’s, and liver
  • Primarily, Plasma Cholinesterase rapidly metabolizes LA
27
Q

How are amides metabolized?

A
  • occurs primarily in liver
  • microsomal cytochrome P-450 enzyme
  • dependent on hepatic blood flow and enzyme availability
28
Q

What are the two most common ways that toxicity occurs?

A
  • inadvertent intravascular injection

- absorption of large amounts of drug from a nerve block that requires large volume

29
Q

LAST stands for what and what 5 things are affected?

A
  • Local anesthetic systemic toxicity (seen 5-10min)
  • CNS
  • CV
  • Allergic Reaction
  • Methemoglobinemia
  • Local tissue
30
Q

CNS effects of LAST

A

Mild = tongue numbness, apprehension, restlessness

Moderate = peri-oral tingling, tremors, slurred speech, drowsiness

Severe = Seizures, cardiorespiratory depression, coma, death

31
Q

CV LAST effects

A
  • palpitations
  • HTN
  • ventricular dysrhythmias
  • myocardial depression
  • bradycardia
  • hypotension
  • CV collapse
32
Q

PVS LAST effects

A
  • low concentrations-vasoconstriction and increased SVR

- as doses increases significant vasodilation and hypotension occurs

33
Q

Arrythmias with LAST

A

-LAST effects electrophysiologic and contractile forces

  • increased PR interval and QRS durations
  • complete AV block, bradycardia, cardiac arrest
34
Q

What preservative is associated with allergic reactions to LA?

A

More common in esters due to para-aminobenzoic acid

35
Q

Which three LA can cause Methemoglobinemia?

A
  • Prilocaine (citanest)
  • Benzacaine
  • Cetacaine
36
Q

What is the metabolite that causes methemoglobinemia and what are the s/s?

A
  • o-toluidine oxidizes hgb to met-hgb
  • tachypnea
  • metabolic acidosis
  • brownish-gray cyanosis
37
Q

Met-Hgb treatment

A
  • Spontaneous is 2-3 hrs

- methylene blue 1mg/kg

38
Q

LAST treatment

A
  • Airway mgt
  • seizure suppresion
  • CPR
  • alert nearest facility with bypass capabilities
  • give IV intralipid
39
Q

Intralipid dosing

A
  • Bolus: 20% intralipid 1.5ml/kg over 1 min
  • Cont: 0.25ml/kg/min
  • Double infusion if BP returns but stays low
  • Continue infusion for a minimum of 30 min

MTSA Orientation Test 2 (2 decks)

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