midterm guide Flashcards
Is Zygomatic Implant immediate, early, delay, or second stage loading?
immediate
What’s the recommended radiographic examination for work up of a zygo implant?
Recommended Radiograph
Panorex: Anatomic structure and pathology detection
Intraoral PA: supplement Panorex
Lateral Cephalometric: Sagittal relationship of jaws
**CT: **Bone volume (width and height) assessment
all 4
Classic Treatment planning requirement for Zygomatic implant placement is
Traditional use of zygoma implants dictates room for
at least TWO conventional implants at anterior
maxilla
Intracrestal lift
* How much can you expect to lift?
1-2mm
Intracrestal lift
Recommended initial Maxillary residual ridge for the most predictable result is ?
bone height 4-6mm
Lateral window lift
* What’s the indication?
Less than 4 mm native maxillary alveolar bone
What’s Schneiderian Membrane?
pseudostratified columnar epithelium of the maxillary sinus overlying connective tissue and periosteum
Membrane can support elevation in the sinus cavity of 4-8mm
limiting factor of sinus lift
Alveolar Ridge Splitting
* What’s the indication and minimum ridge width?
* implant placement?
tx time?
cost?
Barrier membrane?
dif in arches?
Simultaneous implant placement for horizontal bone def
Reduced treatment time
Reduced cost of surgery
Barrier membrane usually not needed minimum width: 2-4mm (pref more than or equal to 3mm)
Maxilla is more applicable: Due to bone type (3 or 4), especially for immeadiate
delayed works well for mandible
used when graft fails/pt doesnt want graft
how much bone should surround implant in ridge splitting
1mm at B/P regions
disadvantages of ridge splitting
Bone loss
Difficult on single tooth site
Cannot Correct Vertical defect
Only ↑alveolar width
Implant placed tends to situated facially due to remodeling and resportion of buccal plate
Various types of bone graft materials
autograft
allograft
xenograft
alloplast
bone types based on hardness
integration times based on bone type
properties of bone grafts
osteogenesis, osteoinduction, osteoconduction
osteogenesis
- viable cells contribute to new bone formation
osteoinduction
- proteins, factors, hormones modulate host cells
osteoconduction
- matrix/scaffold onto which new bone can form
autogenous bone graft
- from?
- preffered? properties?
- donor sites
- forms?
- Cortical vs. Cancellous?
- Same individual
- Gold standard : Osteogenic, osteoinductive, & osteoconductive
- Extra-oral vs. intra-oral donor sites
- Intra-membraneous vs. cartilaginous
- Block vs. particulate forms
- Cortical vs. Cancellous
cons of autogenous
- Need for second operative site
- Insufficient amount of bone
cortical autogenous graft advantages
more bone morphogenic proteins (BMPs) & better structural support
cancellous autogenous graft advantage
more osteoblast precursor cells for greater osteogenic potential
healing time of autogenous graft
Healing time 3~7months
extra oral autogenous donor sites
skull, ribs, illiac crest, tibia
intra oral autogenous sites
man symphasis
ramus
allogratft
- From?
*properties - Types of Allografts?
- From other individuals of the same species
- Cadavers
- Tissue bank
* Osteoinduction & osteoconduction - Types of Allografts
- Freeze-dried bone allograft (FDBA): 6-15 months
- Demineralized freeze-dried (DFDBA) 6 months
- Irradiated bone (2.5 million rads)
allograft advantages
- available?
- Eliminates?
- Reduced?
- Decreases?.
- Fewer?
- Ready availability
- Eliminate second surgery
- Reduced anesthesis & surgical time
- Decrease blood loss
- Fewer complication
allograft disadvantages
- Associated with the use of
tissues from another person - Immune responses
xenograft
- from?
- what is it?
- Highly?
- Rapid revitalized through?
- resorbtion?
- Different species
- Anorganic bone treated to remove its organic component
- Highly osteoconductive
- Rapid revitalized through new blood vessels
- Slowly resorbing matrix structure (6 months ~)
alloplasts properties
* Natural or Synthetic?
* Mostlywhat property?
* Variety of?
* Crystalline or amorphous?
* Granular or molded?
* take longer to?
- Natural or Synthetic
- Mostly osteoconductive
- Variety of textures, sizes, and shapes
- Crystalline or amorphous
- Granular or molded
- take longer to absorb
Type of Alloplastic Bone Graft material
I. Ceramic : HA, TCP
II. Calcium Carbonate : Bio Coral
III. Biocompatible composite polymer
IV. Bioactive glass ceramic : Bio-glass
barrier membrane characteristics
Biocompatible?
Stability for?
Manipulable?
closure form?
Biocompatible
Stability for space maintenance
Manipulability
Primary closure throughout healing period is essential to GBR outcome
non-resorb barrier membranes
GOldstandard for?
Optimal?
Polytetrafluoroethylene (e-PTFE, TR e-PTFE), or titanium mesh
* Titanium Reinforced PTFE Membranes (TR e-PTFE), Ti-Enforced microporous (ePTFE)
Gold standard for GBR
Optimal graft containment
nonresorb barrier mem cons
flap management
- 2nd surgical procedure to remove membrane
natural resorb barrier membranes
made of?
- degrades?
- Limited ability to?
- retention time frame?
Natural: collagen of animal origin
- Enzymatic degradation
- Limited ability to maintain space
- 4 to 6 months of retention
types of resorb barrier mem and resorb time frames
synthetic resorb barrier mem, made of?
- Degradation by?
- rate of membrane resorption?
Synthetic: poly(lactic) and poly(glycolic) acid copolymers
- Degradation by hydrolysis
- Highly variable rate of membrane resorption (pH & material composition)
available bone augmentation procedures
what is GBR
ingrowth of
osteogenic cells
while preventing
migration of
unwanted cells
Benzodiazepines General properties
Benzodiazepines cause
Sedation
Anxiolysis
Muscle relaxation
Anterograde amnesia
Anticonvulsant effects
Benzodiazepines General properties
Common Side Effects
Fatigue
Drowsiness
Respiratory depression !
No direct analgesic Effect
benzos
What receptor does it work on?
Enhances inhibitory effect of neurotransmitters
Facilitates GABA receptor binding
↑membrane conductance of Chloride ions
benzo
reversal agent
Flumazenil (Romazicon)
Competitive antagonist of benzodiazepine receptors (GABA)
Propofol / Diprivan
Mechanism of action, results in?
Enhance GABA inhibitory function = ↑Cl channel = hyperpolarization of cell membrane
Results Rapid onset of unconsciousness
Propofol / Diprivan additional effect?
largely replacing?
Arterial and venous dilatation
Largely replacing Thiopental (Barbiturates)
Ketamine
moa
General Anesthesia Medicine
Selective NMDA receptor blocker
ketamine effects
Dissociative, Hallucinogenic and Amnesic Effect
Sympathomimetic medicine
ketamine disadvantages
Hallucinogenic, Nightmare emergence, Increase Salivary flow
opioid receptros effected
mu
kappa
delta
sigma
opioids effect at kappa
Kappa (κ)
Miosis
Sedation
opioids effect at mu
Mu (μ)
μ1 : Analgesia
μ2 : Respiratory Depression
Physical dependence
Muscle rigidity
opioids effect at delta
Delta (δ)
Behavioral response to pain
opioids effect at sigma
Sigma (σ)
Dysphonia
Hallucinations
desiresable effects of opioids
Analgesia
Sedation
Euphoria
Anti-tussive
undesireable effects of opioids
Respiratory Depression
Coma
Emesis
Constipation
Histamine release
Potential for addiction
opioids occular effect
Miosis
Mechanism of action
○ Edinger-Westphal nucleus of Oculomotor nerve
○ Enhanced parasympathetic stimulation
Significance?
○ Most other causes of coma and respiratory depression produce mydriasis (dilation of pupil)
All Addicts demonstrate pin-point pupils
morphine vs fent potentcy
- Fentanyl=100X potency of morphine
*
morphine vs fent metabolism
Morphine: Conjugate with glucuronic acid
○ Morphine-6-glucuronide (potent analgesic)
○ Morphine-3-glucuronide (inactive)
Fent: Inactive metabolite
○ Remember the “end “ of the effect is due to redistribution!!
○ Fentanyl will accumulate in body fat with repeated injections
what additional route of entry can fent use
transdermal along with IV and IM like morphine
fent vs morphine onset and duration
morphine: Onset 5-10mins, peak within 30mins, T ½ 1.5 – 2 hours, Duration of action : 4-6 hours
fent: Onset of action < 60 sec with peak effect in 2 – 5 mins, Duration 30 – 60 mins
fent is much more lipid soluble, morphine less BBB penetration
morphine vs fent elimination
Morphine Elimination:
End product eliminated by kidney
Renal failure patient may have narcosis and vent failure for days !
Fent Elim
Little effect on renal patient
Clearance dependent on hepatic blood flow
morphine vs fent ADRs
Morphine Adverse Effects
Nausea and Vomiting: Stimulate medullary chemoreceptor trigger zone
Severe respiratory depression: Rigid chest syndrome
Histamine Release: May lead to profound drop in BP and systemic vascular resistance
Fent ADRs
No histamine release
Rigid Chest Syndrome: After large drug bolus !!
opioid reversal agent
naloxone/narcan
naloxone moa
Competitive antagonist at opioid receptors
Greater affinity for μ receptors than κ or δ receptors
noloxone dosing
IV administration of 0.4mg IV (Titrate to effect !!!)
naloxone side effects
Abrupt reversal = Excessive catecholamine release
○ tachycardia, hypertension, ventricular irritability
May antagonize Clonidine
Nausea/Vomiting may be observed
naloxone time frames
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
ASA system
System to estimate medical risk
Originally designed for general anesthesia patient
Commonly known as ASA Classification
ASA classes
1,2,3,4,5,6,E
ASA 1
Normal, Healthy patient without systemic disease
ASA 2
Mild systemic disease
asa 3
Severe systemic disease, limits activity but no
incapacitating
asa 4
incapacitating systemic disease that is constant threat to life
asa 5
Not to survive 24 hours with/without operation
asa 6
Brain-dead patient awaits for organ donation
asa e
Emergency operation
Precedes number status ( i.e. ASA E-II)
ASA Classification, Definition
Normal or Usual:
Distress:
Normal or Usual: Ability to climb one flight of stairs or walk 2 level city blocks
Distress: Undue fatigue, shortness of breath, or chest pain
asa 2 examples
Type II or Non insulin dependent diabetes
Well controlled epilepsy ( no seizure in the past year)
Well controlled asthma
Hypothyroid / Hyperthyroid patient under treatment and currently euthyroid
Healthy pregnant female
> 60 y/o patient
Extreme phobic patient
Drug allergy or multiple allergies patient
Systolic 140/159mmHg and diastolic 90-94mmHg
may proceed with tx
asa 3 examples
Type I DM, well controlled patient
Symptomatic thyroid disease patient
>6 months without any residual complication
Myocardial infarction
CVA
BP (169-199) systolic / (95-114) diastolic
Epilepsy: Several seizures per year
Asthma,: Stress / exercise induced / hospitalization
Angina Pectoris (stable angina)
CHF with
orthopnea ( > 2 pillow)
Ankle edema
COPD
ASA III
No S/S of distress at rest, BUT?
tx mod
tx?
No S/S of distress at rest, BUT not under stressful situation
Serious treatment modification is needed
Yellow light for treatment ( proceed with caution
ASA IV
S/S of their medical problem when?
Their medical problem has greater significance than?
OK for ?
If invasive dental treatment is needed?
go ahead?
S/S of their medical problem at REST
Their medical problem has greater significance than
elective dental treatment
OK for non invasive dental emergency treatment
If invasive dental treatment is needed hospital
Red light for treatment ( DON’T Proceed)
asa 4 examples
Unstable Angina
<6 months without any residual complication
Myocardial infarction
CVA
BP >200 systolic / >115 diastolic
Uncontrolled dysrhythmias
Severe CHF or COPD
Wheel chair bound or need supplemental oxygen
Uncontrolled epilepsy
Uncontrolled IDD
ASA V
def
Hospitalized patient with?
dental care?
ASA V
Moribound patient not to expect to survive 24 hours\
Hospitalized patient with end-stage disease
Palliative dental care
Examples of ASA V Patients
Hospital heart valve surgery patients in need of dental
extractions
Hospital patients with end-stage organ disease in need
of palliative dental care
Patient Demographic in asa classes
Patient Demographic
ASA I or II = 85% dental patients
ASA III or IV = 14% dental patients
who started ASA classification
American Society of Anesthesiologists (ASA)
Started in** 1962**
System to estimate medical risk
Originally designed for general anesthesia patient
Commonly known as ASA Classification
Sedation
Definition
Reduction of irritability or agitation by administration of
sedative drugs, generally to facilitate a medical procedure
MO Dental Board sedation types
Moderate Sedation: Enteral, Parenteral, Pediatric
Deep Sedation / General
Site Certificate for each type
Pediatric Patient Definition and sedation allowed
A patient aged twelve (12) or under. The use of preoperative sedatives for children (aged twelve (12) and under) except in extraordinary situations must be avoided due to the risk of unobserved respiratory obstruction during transport by untrained individuals.
Children (aged twelve (12) and under) can become moderately sedated despite the intended level of minimal sedation; should this occur, the guidelines for moderate sedation apply
Minimal Sedation (Anxiolysis)
Minimal sedation (Anxiolysis)—A minimally depressed level of consciousness produced by a pharmacological method, which retains the patient’s ability to independently and continuously maintain an airway and respond normally to tactile stimulation and verbal command. Although **cognitive function and coordination may be modestly impaired, ventilatory and cardiovascular functions are unaffected. **Note: In accord with this particular definition, the drug(s) and/or techniques used should carry a margin of safety wide enough never to render unintended loss of consciousness. Further, patients whose only response is reflex withdrawal from repeated painful stimuli would not be considered to be in a state of minimal sedation. When the intent is minimal sedation for adults, the appropriate initial dosing of a single enteral drug is no more than the maximum recommended dose (MRD) of a drug that can be prescribed for unmonitored home use
NO used with Rx for minimal sedation
Nitrous oxide/oxygen may be used in combination with a single enteral drug in minimal sedation. Nitrous oxide/oxygen when used in combination with sedative agent(s) may produce minimal, moderate, or deep sedation or general anesthesia.
Moderate Sedation (Conscious Sedation)
A drug induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation.
Generally, no interventions are required to maintain a patent airway, and spontaneous ventilation is adequate.
Cardiovascular function is usually maintained.
Deep Sedation
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 in maintaining a patent airway and spontaneous ventilation may be inadequate.
Cardiovascular function is usually maintained.**
Qualified Sedation Provider
Qualified sedation provider—Any of the following who have satisfied the provisions of this rule:
1. A currently licensed dentist in Missouri with a valid permit to administer enteral, parenteral, or pediatric moderate sedation
2. A currently licensed anesthesiologist
3. A currently licensed certified registered nurse anesthetist.
OMS Resident Anesthesia Training
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
Monitoring Equipment for IV sedation
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
stethocpose and BP cuff use
can be used to determine BP/HR in monitoring
Capnography
Monitoring of concentration or partial pressure of CO2
Graph of expiratory CO2 by expired volume
Advantage of capnography
Breath to breath ventilation data
Respiratory effort
Real-time feedback on treatment ( i.e. IV med administration)
Pulse Oximeter
Measures oxygen saturation of arterial blood
Determine percentage of oxyhemoglobin in capillaries
Operates on 650nm and 950nm wave length: oxygenated
(absorbs more infrared light) and deoxy Hb (absorbs more red light) absorb different wavelenghts and the ratio of this is used to determine O2 saturation
What’s the most reliable airway?
endotracheal intubation
Adjunctive airways
* IN IV sedation, what’s the most appropriate adjunctive airways?
Patient Evaluation should be done by….
Should be conducted by the person planning and administering the anesthetic
Medical history questionnaire has different formats?
A tool to gather written information about the patient’s health
Completed by the patient or the patient’s guardian
Simple format which is easy to understand
Two standard formats: short and long
Airway examination prior to IV sedation is ….
* What are the different class?
everything, based on Mallampati Classification
1: soft palate, fauces uvula, ant/post tonsillar pillars
2: soft palate, fauces uvula
3: soft palate, base of uvula
4: only soft palate
Nitrous oxide…… how was it manufactured?
- Nitrous oxide is made from ammonium nitrate via 240oC heat
- NH4NO3 = N2O + 2H2O
- Compressed in cylinder where 30% is liquefied
- N2O must be 97% pure
What’s the special property or characteristic of Nitrous oxide gas to human?
- cns depressant
- second gas effect
- concentration effect
- rapid onset/recovery (insoluble)
- not flammable/explosive but can support this in other agents
- Oxygen of N2O not used by body (not broken down)
- least potent anaesthetic gas
N2O concentrations
- Optimum concentration of N 2O for production of analgesia while maintaining patient cooperation is 35%
- 20%:80% mixture N2O-O 2 10-15mg of morphine
max is 70% N2O
special properties of n2o
concentration effect and second gas effect
CNS depressant
Concentration Effect
- The higher the concentration of the gas inhaled, the more rapidly arterial tension of the gas increases
- Fresh gas will be pushed into the lungs from the anesthesia machine= increase arterial N 2 O arterial tension
- So its important to start the Nitrous slowly and not blast it high in the beginning
2nd Gas Effect
- Occurs when a second inhalation anesthetic is administered along with N 2O-O 2
- Extreme uptake of N 2O will form a vacuum at alveoli that forces other air ( in this case, other inhalational agent) into the lungs
Chronic exposure of nitrous oxide is detrimental to…?
- Inhibits methionine synthetase impair B12 metabolism = decreased Bone Marrow function =Pernicious anemia (Vitamin B12 anemia)
- Long term exposure ( > 24 hr exposure) = transient bone marrow depression
- also causes neurological deficiencies and perihperal neuropathy
ONLY nonorganic compound other than CO2 that has CNS depressant
properties
N2O
size, pressure and color of N2O/O2 cylinder
Full E cylinder has gaseous 750 psi and liquid states
* 750 psi will stay there until the moment of empty tank
blue color
Full E Cylinder is about 1900 psi in gaseous state only, green color
* Psi will decrease as O2 is being used
