Midterm Flashcards

1
Q

Is zygomatic implant immediate, early, delaey, or second stage loading?

A

● It has to be immediate loading → prosthesis must be placed within
48 hours, preferably 24hrs
○ Otherwise, zygomatic implants may not integrate well with zygomatic bone
● Then for the next 3 months → early loading
● 3-6 months → delayed/conventional loading

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2
Q

What’s the recommended radiographic examination for work up?

A

● Pano, intraoral PA, lateral cephalometric (sagittal relationship of jaws), CT

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3
Q

Classic treatment planning requirements for zygomatic implant placement is:
(2)

A

● Indicated when there is not significant bone for conventional implants in all three
zones and pt does not want bone graft
● At least 2 conventional implants required in the anterior maxilla

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4
Q

Intracrestal lift

A

● When you just need to add a little bone so you don’t perforate
the sinus

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5
Q

Intracrestal lift
How much can you expect the lift?

A

● 1-2mm

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6
Q

Intracrestal lift
Recommended initial maxillary residual ridge for the most
predictable result is? (for intracrestal lift) -

A

> 4mm native
maxillary bone

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7
Q

Lateral window lift- more invasive

A

● Open a window and add bone in canine/premolar area
○ 1. Reflect tissue
○ 2. Osteotomy (open a window on anterior sinus region);
open up a doggy door
○ 3. Put bone graft in there (the bone graft material will
sit on top of the Schneiderian membrane
○ Can possibly place an implant the same day depending
on how much native bone you have

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8
Q

Lateral window lift-
What’s the indication?

A

<4mm of native maxillary alveolar bone

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9
Q

What’s Schneiderian Membrane?

A

● The Schneiderian membrane is the mucous membrane that covers the inner part of
the maxillary sinus cavity

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10
Q

Alveolar Ridge Splitting-

A

split ridge bone open and “Squeeze” in implant into that space

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11
Q

Alveolar Ridge Splitting-
What’s the indication and minimum ridge width?

A

● 2-4 mm (prefer >/= 3mm)

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12
Q

Autogeneous -

A

gold standard, from same individual
○ Osteogenic, inductive, & conductive
■ Osteogenesis - viable cells contribute to new bone formation
■ Osteoinductive - proteins, factors, hormones modulate host
cells
■ Osteoconduction - matrix/scaffold onto which new bone
can form
○ Cortical - More bone morphogenic proteins
(BMPs) and better structural support
○ Cancellous - more osteoblast precursor
cells for greater osteogenic potential
○ Healing time - 3-7 months
○ Ramus vs symphysis

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13
Q

Allograft -

A

from individuals of same species (cadaver, tissue bank)
○ Freeze-dried bone
○ Demineralized freeze-dried
○ Irradiated bone
○ Advantages:
■ Readily available, eliminate 2nd surgery, reduced
anesthesia/surgical time, decreased blood loss, fewer
complications
○ Disadvantages:
■ Associated with use of tissues from another person
■ Immune responses

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14
Q

Xenograft -

A

from different species (cow); takes longer to integrate
○ Highly osteoconductive
○ Rapid revitalized through new blood vessels
○ Slowly resorbing matrix structure (~6 months)

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15
Q

Alloplasts -

A

natural or synthetic; takes longer to integrate
○ Mostly osteoconductive
■ Takes a little longer for our body to resorb them away so not
meant for something fast
○ Variety of textures, sizes, shapes
○ Crystalline or amorphous
○ Granular or molded
○ Types:
■ Ceramic
■ Calcium carbonate
■ Biocompatible composite polymer
■ Bioactive glass ceramic
● Need membrane for primary closure throughout healing

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16
Q

How to classify how “hard” the native bone?

A

Type 1 hardest > Type 4 least hard
● Type 1 - almost entirely compact bone
○ Oak wood - expect 5 months to integrate
● Type 2 - thick cortical bone + dense trabecular bone
○ Pine wood - expect 4 months to integrate
● Type 3 - thin cortical bone + dense trabecular bone
○ Balsa wood - 6 months to integrate
● Type 4 - thin cortica bone + low density trabecular bone
○ Styrofoam - 8 months to integrate

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17
Q

Properties of Benzodiazepine? → no direct analgesic effect
● Benzo’s cause:
(5)
● Common Side effects:
(3)

A

○ Sedation
○ Anxiolysis (does not take pain away! Only sleepy! Which is why we
typically use fentanyl and midazolam together)
○ Muscle relaxation
○ Antrograde amnesia
○ Anticonvulsant effects

○ Fatigue
○ Drowsiness
○ RESPIRATORY DEPRESSION!!

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18
Q

Benzodiazepine
What receptor does it work on?

A

→ GABA
● Enhances inhibitory effect of neurotransmitters
○ Facilitates GABA receptor binding
○ Increases membrane conductance of Chloride ions

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19
Q

Reversal Agent?

A

● Flumanzenil (Romazicon) - competitive antagonist of benzodiazepine
receptors
○ Use for reversal of benzo sedation and/or overdose
○ Prompt (<1 min) hypnotic reversal, Amnesia is ?
○ Respiratory depression may linger despite “alert/awake” appearance
○ Dosage
■ IV administration of 0.2mg every min until reversal
Rapid hepatic clearance → repeat dose may be needed in
1-2 hours
■ T ½ is only ~1 hour

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20
Q

Ketamine: → horse tranquilizer

A

● General anesthesia medicine
● Selective NMDA receptor blocker
● Dissociative, hallucinogenic, and amnesic effect
● Sympathomimetic medicine
● Disadvantages:
○ Hallucinogenic
○ Nightmare emergence
○ Increase salivary flow

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21
Q

Propofol:

A

● Mechanism of action:
○ Enhance GABA inhibitory function→ increase Cl channel → increase
hyperpolarization of cell membrane
○ Results rapid onset of unconsciousness
● Arterial and venous dilatation
● Largely replacing Thiopental (barbiturates)

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22
Q

● Mu (4)

A

○ Mu1: Analgesia
○ Mu2: Respiratory depression
○ Physical dependence
○ Muscle rigidity

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23
Q

● Kappa (2)

A

○ Miosis - pin-point pupil
○ Sedation

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24
Q

● Delta
(1)

A

○ Behavioral response to pain

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25
Q

● Sigma
(2)

A

○ Dysphonia (difficulty speaking)
○ Hallucinations

26
Q

● Endogenous peptides interact with opioid receptors
(30

A

○ Endorphins, Enkephalins, Dynorphins

27
Q

Body’s reaction to opioid

A

● Miosis - pin-point pupil
○ Significance? → most other causes of coma and respiratory
depression produce mydriasis (dilation of the pupil)

28
Q

Body’s reaction to opioid
Mechanism of action
(2)

A

■ Edinger-Westphal nucleus of oculomotor nerve
■ Enhanced parasympathetic stimulation

29
Q

Body’s reaction to opioid
● Desirable effect (really want analgesia and sedation with opioid use, but we
must be aware of other ef ects that come with the drug)
(4)

A

○ Analgesia
○ Sedation
○ Euphoria
○ Anti-tussive (relieves a cough)

30
Q

Body’s reaction to opioid
● Undesirable Effect
(2)

A

○ Respiratory depression
○ Coma, emesis, constipation, histamine release, potential for addiction

31
Q

Difference between morphine and fentanyl
● Morphine

A

○ The Gold Standard of pain med
○ Pharmacology
■ IM/IV
■ Hyperpolarize nerve cell, decrease release of substance P
■ Least lipophilic → minimum crossing BBB
■ Onset 5-10 mins, peak within 30 mins
■ T ½ 1.5-2 hours
■ Duration of action: 4-6 hours
■ Do not give to neonate (unable to conjugate)
● Can stay in system for long time
○ Metabolism
■ Conjugate with glucuronic acid
● Morphine-6-glucuronide (potent analgesic)
○ That is why duration is so long, because once
morphine is gone, it is still this analgesic form
working
● Morphine-3-glucuronide (inactive)
○ Elimination
■ End product eliminated by kidney
■ Renal failure patient may have narcosis and vent failure for
days!
○ Adverse Effect
■ Nausea and vomiting
● Stimulate medullary chemoreceptor trigger zone
■ Severe respiratory depression
● Rigid chest syndrome
■ Histamine Release
● May load to profound drop in BP and systemic
vascular resistance

32
Q

Difference between morphine and fentanyl
● Fentanyl

A

○ 100X Potency of morphine
○ Pharmacology
■ Oral/IV/Transdermal
■ Analgesic and Sedative effect
■ High lipid solubility → rapid onset / short duration
■ Onset of action <60 sec with peak effect in 2-5 mins
■ Duration 30-60 mins
○ Metabolism
■ Inactive metabolite
● Remember the “end” of the effect is due to
redistribution!!
● Fentanyl will accumulate in body fat with repeated
injection
○ Elimination
■ Little effect on renal patient
■ Clearance dependent on hepatic blood flow
○ Adverse Effect
■ No histamine release
■ Rigid Chest Syndrome
● After large drug bolus!!

33
Q

Reversal agent?
● Naloxone (Narcan)

A

○ Mechanism of Action
■ Competitive antagonist at opioid receptors
■ Greater affinity for mu receptors than kappa or sigma
receptors
○ Pharmacology
■ Reversal of endogenous or exogenous opioid compound
■ Rapid antagonizing (1-2 min)
■ Brief duration of action (30-45 mins) IV
● Rapid redistribution from CNS
■ T ½ is only 30-80 mins
● Respiratory depression may linger despite
“alert/awake” appearance
○ Dosage
■ IV administration of 0.4mg IV (titrate to effect!!!)
○ Recommended usage
■ Any suspicion
● Support respiration (O2 and continue monitoring)
● Check oxygen saturation, vital signs
■ Continued sluggish response
● Rule out hypoglycemic shock, CVA, psychotic episode
● Consider giving IM, if concern for re-sedation, give
0.4mg IM
○ Side Effects
■ Abrupt reversal → Excessive catecholamine release
● Tachycardia, hypertension, ventricular irritability
■ May antagonize Clonidine
■ Nausea/Vomiting may be observed

34
Q

● ASA I:

A

normal, healthy patient without systemic disease
○ Little or no anxiety patient
○ Tolerate stress with no adequate risk

35
Q

● ASA II:

A

mild systemic disease
○ Healthy but with some blemish
○ Extreme anxiety/fear → distress → chest pain, shortness of breath
○ Older (<60 y.o)
○ Pregnant
○ Green light with CAUTION
○ Well controlled hypothyroid, asthma, epilepsy

36
Q

● ASA III:

A

severe systemic disease, limits activity but no incapacitating
○ No signs/symptoms of distress at rest BUT not under stressful
situation
○ Serious treatment modification is needed
○ Yellow light for treatment (proceed with caution)
○ Ex:
■ Type 1 DM, well controlled
■ Symptomatic thyroid ds, <6 month without residual
complication
● MI, CVA
■ BP (169-199) systolic/ (95-114) diastolic
■ Epilepsy → several seizures per year
■ Hospitalization for asthma
■ Angina (ankle edema, orthopnea <2 pillow), CHF, COPD
(emphysema, chronic bronchitis)

37
Q

● ASA IV:

A

incapacitating systemic disease that is a constant threat to life
○ Signs and symptoms of their medical problem at REST
○ Their medical problem has greater significance than elective dental
treatment
○ OK for non invasive dental treatment
○ If invasive dental tx is needed → Hospital
○ Red light for tx (DON’T proceed)
○ Ex:
■ Unstable angina, <6 months without residual complication
● MI, SVA
■ BP >200 systolic / <115 diastolic
■ Dysarrhythmias uncontrolled
■ Sever CHF or COPD (Requires wheelchair with supplemental
oxygen), uncontrolled epilepsy, Uncontrolled IDDM

38
Q

● ASA V:

A

not to survive 24 hours with/without operation
○ Moribound pt not to expect to survive 245 hours
○ Hospitalized patient with end-stage disease
○ Palliative dental care
○ Hospital heart valve surgery pts in need of dental extractions
○ Hospital pts with end-stage organ disease in need of palliative dental
care

39
Q

● ASA VI:

A

brain-dead patient awaits for organ donation

40
Q

● ASA E:

A

emergency operation
○ Precedes number status (i.e. ASA E-II)

41
Q

Who started the classification?

A

● American Society of Anesthesiologists (ASA) - Started in 1962

42
Q

Sedation laws in missouri
● (FOR REAL, we ALL need to know it. It’s the matter of life and death)”

A

● Reduction of irritability or agitation by administration of sedative drugs,
generally to facilitate a medical procedure

43
Q

Things that you NEED licensure for:
1. Moderate Sedation (need individual certificate for each part of
moderate sedation as well)

A

a) Enteral
b) Parenteral
c) Pediatric (hardest part)- pt aged 12 or under
i) The use of preoperative sedatives for children except
in extraordinary situations must be avoided due to
the risk of unobserved respiratory obstruction during
transport by untrained individuals.
ii) Children under age 12 can become moderately
sedated despite the intended level of minimal
sedation; should this occur, the guidelines for
moderate sedation apply.
1) So you are accountable if something goes
south because it will be as if you are giving
them moderate sedation without a license.
2) Don’t mess with children unless you’re
trained.
iii) Minimal sedation is okay - nitrous
1) As long as you INTEND on minimal sedation
for adults, nitrous can be used and you cannot
go over the max dose

44
Q
  1. Deep Sedation/General Anesthesia
A

■ A drug-induced depression of consciousness during which
patients cannot be easily aroused but respond purposefully
following repeated or painful stimulation.
■ The ability to independently maintain ventilatory function
may be impaired.
■ Patients may require assistance to maintaining a patient
airway and spontaneous ventilation may be inadequate.
■ Who can do this?
● AEGD created by ADA
● OMS or Dental Anesthesiologist training program
● AMA or AOA
● Also need ACLS (advanced cardiac life support and 15
hours of board approved continuing education
pertaining to medical emergencies, etc.

45
Q
  1. Site Certificate for each type
A

■ Office site has to have it as well!

46
Q

Qualified Sedation Provider

A

○ Any of the following who have satisfied the provisions of this rule:
■ A currently licensed dentist in Missouri with a valid permit to
administer enteral, parenteral, or pediatric moderate
sedation.
■ A currently licensed anesthesiologist.
■ A currently certified registered nurse anesthetist.

47
Q

OMS anesthesia training requirement

A

● FIVE months of anesthesia training
○ Minimum of consecutive 4 months, OMS must function as an anesthesia
resident with commensurate level of responsibility.
○ One month of pediatric anesthesia
● Senior resident must have at least 150+ office based sedation cases

48
Q

All the monitoring equipment used in IV sedation
(5)

A

● Device to measure blood pressure and heart rate with multiple size cuffs
○ To auscultate the heart and lungs
● Pulse oximetry with appropriate probes
● Electrocardiogram
● Temperature monitor
○ Ideal that monitor can print

49
Q

How does each one of those equipment works?
● DRE Machine
(3)

A

○ EKG, BP, Capnography

50
Q

Capnography
Know how it works including what it is measuring?
(3)

A

● Monitoring of concentration or partial pressure of CO2
● Graph of expiratory CO2 by expired volume
● Advantage → breath to breath ventilation data, respiratory effort, real-time
feedback on treatment (IV med administration)

51
Q

Pulse oximeter
How does that red light work?
(3)

A

● Measures oxygen saturation of arterial blood
● Determines percentage of oxyhemoglobin in capillaries
● Operates on 650nm and 950nm wavelength
○ Use this wavelength to calculate oxygenated hemoglobin vs reduced
hemoglobin to calculate how much partial pressure the oxygen is in
your finger tip

52
Q

Definitive airways
What’s the most reliable airways
● Oral intubation?

A

○ Endotracheal intubation

53
Q

Adjunctive airways
In IV sedation, what’s the most appropriate adjunctive airways?

A

● Nasal cannula?
○ No airtight seal
○ Significant air dilution
○ Cannot be scavenged
○ No N2O, inhalation agents
○ No reservoir bag
○ Often uncomfortable

54
Q

Patient evaluation should be done by…

A

● The person planning and administering the anesthetic (that’s you, doctor!!!)

55
Q

Medical history questionnaire has different formats?

A

● Completed by the patient or the patient’s guardian
● 2 Standard formats:
○ Short format
○ Long format

56
Q

Airway examination prior to IV sedation is…
What are the different class?

A
57
Q

Nitrous oxide… how was it manufactured?

A

● o Made from ammonium nitrate heated up to 240 degrees celcius (Not sure if this is
the answer he was looking for)
○ NH4NO3 → N2O + 2H2O
○ Compressed in cylinder where 30% is liquefied
○ N2O must be 97% pure (Not N2, NO, NO2, NH4, CO, etc)
■ Worst most dangerous is CO → reacts with water vapor to form acid
which damages pulmonary epithelium → pulmonary edema
● N2O is also anhydrous

58
Q

What’s the special property or characteristic of nitrous oxide gas to human?

A

● Only non-organic compound other than CO2 that has CNS depressant properties
● Only inorganic anesthetic gas in clinical use
● Concentration Effect
○ Higher concentration – more rapid arterial tension of gas increases → so GO
SLOW
● If you push dial so fast, nitrous can form a vacuum at alveoli that forces other air into
lungs = SECOND GAS EFFECT
● Capable of oxygen supporting combustion
● Effect on organ systems
○ Cardiovacular
■ Stimulation of catecholamine yet myocardial depression
○ Respiratory
■ Stimulation of catecholamine
● Tachypnea and decrease tidal volume
○ Renal
■ Reduce urine output
● Toxicity
○ Prolong exposure Bone marrow depression, neurological deficiencies
peripheral neuropathies and pernicious anemia

59
Q

Chronic exposure of nitrous oxide is detrimental to…?

A

● To health of dental personnel

60
Q

Know a few things about gas cylinder such as size, pressure, and color?
(5)

A

● Green: oxygen
● Blue: NO
● Portable units use E cylinder
● Oxygen is about 1900 psi
● NO is 750 psi

61
Q

I have one history question on the exam.

A

● Nitrous started in 1776 - Joseph Priestly discovered N2O
○ Couple years later he found O2 as well
● 1795 - Sir Humphrey Davy wrote a book about procedure with N2O
● 1841 Horace Wells, William Morton started dental practice in Bosting using N2O
● 1842 Crawford Long uses ether to remove tumor in GA
○ In different countries, people are trying different things
● 1844 Gardner Colton demonstrated N20 - Good thing
● 1844 Colton had John Riggs extract Horace Wells tooth using N2O (Morton was an
audience that day)
● 1845 Horace Wells demonstrated N2O at Harvard Medical School
● 1846 Morton demonstrated use of ether at Ether dome in Boston
● As time goes on, people are using ether and chloroform instead of N2O until 1863
N2O was reintroduced by Colton
○ He was doing 100% nitrous - yikes
■ 120k pts without death
● 1868 Edmund Andrews started adding oxygen into nitrous treatment (20% O2)
● 1930s → most dentists using 80% N2O
● 1945 introduce lidocaine to replace N2O
● N2O then turned into anxiolytic and sedative usage
● 1976 ADA mandates inhalation sedation device to deliver no less than O2
atmospheric concentration