• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/17

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

17 Cards in this Set

  • Front
  • Back
1) Definition of anxiety. Subjective or objective?
2) Definition of fear. Subjective or objective?
3) Definition of phobia
4) Definition of pain?
5) What is more common in dentistry, anxiety or fear?
6) How is the pain threshold affected by anxiety and psychological perception?
1) Feeling of apprehension, the source of which may be vague or unknown. Subjective
2) Feeling of apprehension, source is known. Objective
3) Persistent and irrational fear of something specific that results in avoidance behavior
4) Unpleasant SENSORY and EMOTIONAL experience arising from actual or potential tissue damage. Includes the perception of an uncomfortable stimulus and the response to that perception
5) Anxiety
6) It can be raised or lowered by these things alone. Anxiety is a great modulator of pain
1) What are the top 3 things ranked by dentists for pain and unpleasantness for patients?
2) What is the pain management dilemma?
3) Nakai's study on local anesthesia effectiveness in pediatric dental offices says observers report ineffective anesthesia (__%) of the time, and dentists report is (___%) of the time
4) Nakai's study correlated LA ineffectiveness with what 2 things?
1) Drilling without anesthetic and excavating caries without anesthetic is #1, #2 is receiving an injection
2) To eliminate procedure pain, one must first inflict injection pain
3) Observer - 12%. Dentist - 8%
4) Pre-op pain and anxiety, major dental procedures (pulp therapy and extractions)
1) Every local anesthetic agent has the potential for depressing what?
2) What is pathognomonic for a drug overdose?
3) 3 causes of lidocaine toxicity?
4) What are the 2 different times of onset for toxicity, and what are they caused by?
1) The CNS
2) Seizures
3) Rapid vascular absorption, intravascular injection, overdose
4) Immediate (<5 min), caused by intravascular injection or rapid vascular absorption because of no vasoconstrictor

Delayed (5-15 min), cause by an overdose
1) Doses of LA below what concentration can be therapeutic? Doses above what concentration causes convulsions?
2) Explain the biphasic system effects of lidocaine
3) What comes first - respiratory depression or cardiovascular?
4) What potentiates toxicity?
5) In mild toxicity, is the excitatory or inhibitory pathway depressed first?
1) Below 5 ug/mL = therapeutic, >8 ug/mL = convulsions
2) At low levels: excitatory. At high levels: inhibitory
3) Respiratory (you're not going to drop dead, you'll droop dead)
4) Respiratory depression (acidosis)
5) Inhibitory
1) Does mild toxicity have excitatory or inhibitory signs and symptoms? What are they?
2) What happens to vital signs during mild toxicity?
3) Lots of mild toxicity signs can be disguised by what effects?
1) Excitatory. Headache, dizziness, confusion, talkativeness, apprehension, excitedness, blurred vision, slurred speech, ringing in ears (tinnitus), irrational conversation
2) Everything elevated (HR, RR, BP)
3) Effects of nitrous (blurred vision, slurred speech, ringing in ears)
List signs and symptoms of low to moderate overdose levels
Signs - confusion, talkativeness, apprehension, excitedness, slurred speech, stutter, muscular twitching, nystagmus, HTN, tachycardia/tachypnea

Symptoms - headache, lightheadedness, vertigo, blurred vision, ringing in ears, numbness of perioral tissues, flushed or chilled feeling, drowsiness, disorientation, loss of consciousness
1) Does severe toxicity have excitatory or inhibitory signs and symptoms? What are they?
2) What is the major sign of severe toxicity and not allergic reactions? Describe the 3 phases
1) Inhibitory - generalized tonic-clonic seizure, generalized CNS depression, depressed vitals, respiratory depression, apnea, cardiovascular collapse and death
2) Tonic-clonic seizures. 1. Tonic phase (lose consciousness and have muscle rigidness 10-20 seconds), 2. Clonic phase (repetitive contractiosn and relaxation of skeletal mucles). 3. Postictal phase - cardiovascular and respiratory depression 10-30 minutes
List the 6 things that happen with moderate to high blood levels of LA (toxicity)
Generalized tonic-clonic seizures => generalized CNS depression => hypotension => bradycardia => respiratory depression => hypoxemia
1) Toxicity-induced CNS depression progresses to ____ and ____
2) What happens to levels of pCO2?
3) 3 ways this affects drug toxicity?
4) How do seizures affect respiratory acidosis?
1) Respiratory depression, hypogemia
2) Levels of pCO2 rise (lowered pH, respiratory acidosis)
3) Increases drug toxicity. 1) shunts blood to brain, away from liver, 2) get decreased plasma protein binding of agent (proteins RELEASE the lidocaine to the bloodstream because it's more acidic) 3) decreases seizure threshold (enhanced by narcotics)
4) Further enhance it, so downward spiral of events intensifies with increasing serum lidocaine levels
1) How does decreasing serum pH affect plasma protein binding of lidocaine? At pH 7.6, what % is bound? At 7.0, what % is?
2) List 3 medications competing with lidocaine plasma protein binding and what they do
3) Why are children more at risk for toxicity? A young child at 15 kg has __% adult blood volume
4) What is the best measurement for determining how much LA a kid can take? What is the problem with obese kids?
1) Reduces it. 60%, 35%
2) Triple DQ - Demerol (analgesic/sedative), Dilantin (anticonvulsant), Desipramine (tricyclic antidepressant), Quinidine (antiarrythmic)
3) Lesser blood volume than adults - 20-30% of adult blood volume
4) Blood volume, but since we can't measure it, we use weight (best representation of blood volume). With obese kids, weight is NOT representative, so use age based instead of weight based
1) 3 causes of slow vascular lidocaine removal?
2) Patients don't usually die until you reach __x MRD
3) What is one advanced intervention for lidocaine toxicity management?
1) Impaired circulation, geenral health compromise (serum levels are 2x healthy subjects), congestive heart disease (decrease renal circulation), hepatic or renal dysfunction
2) 3x
3) 20% lipid emlusion, must be given intravenously - bolus followed by IV infusion. Used in severe overdose situations associated with cardiovascular collapse. Only adult case reports published to date, no studies involving children
What is the protocol for lidocaine toxicity management? (5 steps). Why do you give O2?
1. Position - supine in the unresponsive sedated patient, neck/shoulder roll for unobstructed, patent airway
2. Circulation - usually adequate, hypotension and tachycardia need BLS intervention
3. Airway - usually adequately maintained, follow precautions for hypoxia
4. Breathing - usually maintained, may be depressed or absent (bag/mask/valve)
5. Definitive - continue observation/monitoring vital signs, EMS activation with transport and observation

MAINTAIN AIRWAY AND GIVE O2 because lowers carbon dioxide levels, brings pH back to normal so reverses respiratory acidosis
How do you measure a seizure?
1. Circulation - Usually not affected, except in cases of extreme hypoxia
2. Position/Airway - put nothing in mouth unless to open airway/remove anything in mouth/move all equipment from patient area
3. Breathing - usually not affected, but bag/valve/mask if not
4. Definitive (status epilecticus - seizure for 5 mins +)
- IN Midazolam (0.2-0.3 mg/kg) ***
- IM Midazolam (0.5 mg)
IV Diazepam 2-20 mg (0.1-0.3 mg/kg IV), titrate 5 mg/min
IV midazolam (1 mg/min titration)

EMS notification and transport
6 factors contributing to increased risk of local anesthetic overdose
HMM, Vasoconstrictors Should be Standard!

1. High concentration solution used
2. Multiple quadrants treated during one appointment
3. MRD not calculated by weight
4. LA without Vasoconstrictors used
5. Sedatives used comcomitantly (especially opioids)
6. Standard volume per injection
1. What does the council on dental therapeutics say about max lidocaine dosage?
2. Do you need to reduce articaine dosages?
1. If narcotic analgesics/sedatives are combined with lidocaine, dosage should be reduced to 2 mg/lb (4.4 mg/kg) for children six years old and younger
2. No, because of the way it's metabolized
5 steps to prevent lidocaine toxicity?
MA Says Post-injection observation, Recognition

1) MRD not exceeded
2) Aspirate/inject slowly
3) Smallest dose with most accurate technique that will yield highest success
4) Post-injection observation for first 5 minutes (will tell you if there’s been rapid systemic absorption or intravascular injection)
5) Recognize early signs of toxicity and provide appropriate management (BLS + O2)
1) What is oraverse and how does it work?
2) What does pharmokinetics reveal immediately after administration?
3) Should you use this for a LA overdose?
1) Phentolamine Mesylate, for patients >6 y/o, non-selective alpha adrenergic antagonist (causes vasodilation at site of admin). Binds epi, lido goes into bloodstream
2) Second peak in lidocaine
3) NO - this will cause an increase in blood concentration of LA!