Test One: LA And Fluoride Flashcards

0
Q

What is the purpose of the benzene ring in the LA structure?

A

It is lipophilic which aids in crossing biological membranes

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1
Q

What is the difference between an amide and an ester linkage for local anesthetics?

A

Metabolism and clinical efficacy; esters metabolized in tissue/plasma by plasma cholinesterase making it easier to cleave and inactivate, also higher chance of allergy

Amides metabolized in Liver

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2
Q

Once inside the membranes how does the structure change?

A

Proton added to the tertiary amine at the other end to make it water soluble/polar

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3
Q

What is the mechanism of action of LAs?

A

Blocks action potentials by blocking sodium channels in the BH+ form

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4
Q

What is within a carpule of anesthesia?

A

Epinephrine, HCl or NaOH to adjust pH of solution, and metabisulfite (antioxidant to increase shelf life–cause of most allergies), isotonic NaCl

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5
Q

Theories for mode of action on sodium channels

A

Membrane expansion theory: Incorporation into the membrane closes pores/passage of electrolytes
Receptor mechanism: physical occlusion, allosteric change in conformation
alteration of electrical field

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6
Q

What phase of an action potential is affected by locals?

A

Phase 0-greatest influx of sodium ions; does not affect resting membrane potential

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7
Q

What is a differential nerve blockade?

A

Loss of autonomic influence by blocking temp sensation, pain, touch, pressure, and motor function

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8
Q

Why does cocaine not need epinephrine for vasoconstriction?

A

Cocaine prevents the reuptake of NTs which causes vasoconstriction

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9
Q

How does infection/inflammation affect locals?

A

Lower pH in tissue, increased blood flow promoting clearance, alteration in Na channel function and number, increased response to noxious stimulants

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10
Q

What processes do amides undergo during biotransformation?

A

Hepatic microsomal metabolism: Dealkylation and glucuronidation (any liver disease or decrease of hepatic circulation can cause systemic intolerance)

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11
Q

Why does articaine have a low risk of toxicity?

A

Its ester side chain is metabolized in plasma very quickly

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12
Q

How does renal clearance relate to protein binding capacity and pH of urine?

A

Inverse relationship with binding and inversely proportional to pH

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13
Q

What effect do LAs have on the heart and why?

A

They can cause decreased contractility. Bupivicaine is a highly lipophilic anesthetic and wants to affect excitable tissue like the myocardium- can be cardiotoxic

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14
Q

Most serious consequence of systemic LA toxicity?

A

postconvulsive central nervous system depression

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15
Q

What are some adverse effects of intravascular injection of a LA?

A

Cardio and resp depression, neuro damage and death

16
Q

What is Clark’s rule for dosage?

A

Based on body weight. For a child: (weight in lbs. x adult dose)/ 150

17
Q

What is the max dose for xylocaine/lidocaine?

A

With epi: 7 mg/kg or 500 mg

Without epi: 4.5 mg/kg or 300 mg

18
Q

What is an adverse effect of prilocaine?

A

Methemoglobinemia: reduced capacity of hemoglobin to carry oxygen (also articaine and benzocaine)

19
Q

Why is bupivicaine not recommended for children or disabled people?

A

More potent and maybe toxic than lido; prolonged effect and greater potential for soft tissue injury

20
Q

What is a risk associated with 4% articaine and prilocaine?

A

Greater possibility of paresthesia

21
Q

What is the reversal agent for LA effects?

A

Phentolamine mesylate (OraVerse): Alpha adrenergic blocker

22
Q

What is epinephrine reversal?

A

Hypotension. This can be caused by antipsychotics like Prazosine which is an alpha1 blocker

23
Q

EMLA

A

Eugenic mixture of local anesthetics; topical cream for skin–2.5% lidocaine and prilocaine

24
Q

Oraqix

A

Intraoral preparation of EMLA- 50% pain reduction for srp

25
Q

Probable toxic dose for fluoride?

A

5 mg/kg-minimum dose that could cause life threatening systemic signs/symptoms

26
Q

Mechanism of action of fluoride

A
  • inhibit enamel demineralization
  • enhance enamel remineralization
  • inhibit metabolism of carbs in cariogenic bacteria
27
Q

Tx for acute fluoride toxicity

A
  • prevent further absorption with gastric levage using fluid high in Ca like milk
  • cardiopulmonary monitoring
  • blood analysis
  • iv infusion of salts like calcium gluconate as a buffer
  • alkaline diuresis to promote excretion
28
Q

Where and how does fluorosis (chronic toxicity) occur?

A

Excess ingestion of fluoride during development of teeth. Most commonly permanent canines and premolars and second molars. Once crowns are completely formed fluorosis is not possible.

29
Q

Fluoride poisoning signs

A

Nausea, vomiting, diarrhea, can progress to hypotension, hypocalcemia, and hypomagnesemia and acidosis–>severe cardiac dysfunction

30
Q

What concept is fluoridation of communal water supplies fulfilling?

A

Low concentration, high frequency

31
Q

Optimal fluoride concentration in cold, cool, and warm climate areas

A

Cold- 1.2 ppm
Cooler- 1.0 ppm (60% of pop has access to this concentration)
Warmer- 0.6-0.8 ppm

32
Q

What is the recommended fluoride concentration in schools and why is it different?

A

4.5 x higher than community because kids spend 1/4 of their time in school and they need to compensate for this lack of community exposure during these times

33
Q

What does dosage of prescribed fluoride supplements depend on?

A

Age and existing fluoride concentration in water supply

34
Q

What are the 3 fluoride formulations?

A

APF (acidulated phosphate fluoride), sodium fluoride, and stannous fluoride

35
Q

Which formulation of fluoride is preferred?

A

APF