PhamBam Flashcards

1
Q

Primary HyperPTH diagnostic test?

A

ELEVATED PTH and Calcium
Remember, asymptomatic hypercalcemia and Nephrolithiasis

The most common clinical presentation of primary hyperparathyroidism (PHPT) is asymptomatic hypercalcemia. The diagnosis is usually first suspected because of the incidental finding of an elevated serum calcium concentration on biochemical screening tests. In addition, PHPT may be suspected in a patient with nephrolithiasis.
If hypercalcemia is confirmed, intact parathyroid hormone (PTH) should be measured concomitantly with the serum calcium. PHPT is diagnosed by finding a frankly elevated PTH concentration in a patient with hypercalcemia. When the PTH is only minimally elevated or within the normal range (but inappropriately normal given the patient’s hypercalcemia), PHPT remains the most likely diagnosis, although familial hypocalciuric hypercalcemia (FHH), a rare disorder, is possible (Uptodate)
PTH serum levels is the answer

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2
Q

Primary hyperPTH phosphate?

A

= low phosphate

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3
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic Kidney disease?

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4
Q

In primary hyperparathyroidism, what is the calcium, phosphate & all phos labs look like

A

Primary Hyperparathyroidism-Calcium is high and phosphate is low

Calcium and Phosphate always go in opposite directions, if one if high the other is low, because if both are higher they can crystalize in the blood so body prevents this at all costs.

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5
Q

In secondary hyperparathyroidism, what is the calcium, phosphate & all phos labs look like

A

Secondary Hyperparathyroidism-Calcium is low and phosphate is high. All phosphate is normal

Calcium and Phosphate always go in opposite directions, if one if high the other is low, because if both are higher they can crystalize in the blood so body prevents this at all costs.

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6
Q

In paraneoplastic hyperparathyroidism, what is the calcium, phosphate & all phos labs look like

A

Paraneoplastic Hyperparathyroidism-Calcium is high and phosphate is low. Alk phosphate is norm

Calcium and Phosphate always go in opposite directions, if one if high the other is low, because if both are higher they can crystalize in the blood so body prevents this at all costs.

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7
Q

Describe calcium phosphate, and all phos levels in…

Paget’s Disease
Cherubsim
Fibrous Dysplasia
Ossifying firm

A

Calcium and Phosphate always go in opposite directions, if one if high the other is low, because if both are higher they can crystalize in the blood so body prevents this at all costs.

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8
Q
  1. Obstructive and restrictive lung disease similarity?
A

SAME TIDAL VOLUME
= reduced FEV1, unchanged TV, SOB with exertion and

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9
Q

What is the difference between Obstructive and Restrictive/obesity lung volumes

A

Obstructive = decreased FEV1/FVC. Increased residual volume, functional residual capacity, and (?) tidal volume. Restrictive/Obesity = normal to increased FEV1/FVC ratio. Decreased TLC, RFC, and RV.

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10
Q

Difference between obstruction and restrictive lung diseases

A

Looks like total lung capacity in obstructive lung disease is higher.

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11
Q
  1. What is Protein C?
A

STRONG PHYSIOLOGIC ANTICOAGULANT

Serine protease; Autoprothrombin IIa and blood coagulation factor XIV. Inactivates factor Va and VIIIa in anticoagulation.

Protein C is produced in the liver, and is Vit K dependant, and part of the regulation of the clotting cascade, it is activated when coming into contact with active thrombin in the blood. Test answer potent anticoagulant

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12
Q
  1. First degree block treatment?
A

PACEMAKER

= Asymptomatic patients with first degree AV block do not require any specific therapy.
= The rare patient with first degree AV block and symptoms consistent with the loss of atrioventricular synchrony, a situation sometimes referred to as “pacemaker syndrome,” is a potential candidate for a pacemaker. Other

situations in which a pacemaker may be considered for first degree AV block include patients with concurrent neuromuscular disease and patients with a wide QRS complex with suspected conduction delay below the AV node.

First degree is increased PR interval of over .2 seconds

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13
Q
  1. Reversible asthma FEV? = answer 12% and 200mL
A

= Reversibility is present if there is at least a 12% and 200mL increase in the FEV1 after bronchodilator given.

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14
Q

Multiple sclerosis = answer was 3 key words

A

Auto immune central demyelination

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15
Q
  1. Serotonin syndrome treatment?
A

Cyproheptadine H1 antagonist (antihistamine)

At high concentrations, has antiserotonergic (5HT2 – excellent for tx of SS), anticholinergic, antidopaminergic effects.

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16
Q

Symptoms of Serotonin Syndrome:

A

tremors, myoclonus, hyperreflexia, mydriasis, GI symptoms (N/V/D).

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17
Q

Five principles are central to the management of serotonin syndrome:

A
  • Discontinuation of all serotonergic agents
  • Supportive care aimed at normalization of vital signs
  • Sedation with benzodiazepines
  • Administration of serotonin antagonists
  • Assessment of the need to resume use of causative serotonergic agents after resolution of symptoms
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18
Q

Which drug may induce Serotonin syndrome when combined with a selective serotonin reuptake inhibitor.

Alafentanil
Fentanyl
Meperiidine
Morphine

A

Meperidine

Serotonin syndrome is characterized by confusion agitation tachycardia, fever, hyperreflexia, mydriasis, myoclonus. Normeperidine is an active metabolite of meperidine

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19
Q
  1. Transfusion related complication?
A

Transfusion-related acute lung injury (TRALI) = uncommon syndrome due to the presence of leukocyte antibodies in transfused plasma. TRALI is believed to occur in approximately one in every 5000 transfusions.
Leukoagglutination and pooling of granulocytes in the lungs may occur, with release of the contents of leukocyte granules, and resulting injury to cellular membranes, endothelial surfaces, and potentially to lung parenchyma. Management of the patient with TRALI includes immediate discontinuation of the transfusion and reporting to the blood bank that TRALI is suspected. Therapy is supportive with supplemental oxygen and ventilatory support with lung protective strategies when clinically indicated. Although the risk for mortality is significant, patients who survive a TRALI episode are generally expected to recover completely.

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20
Q
  1. Phenytoin and Tylenol toxicity
A

Answer was something to do with enzyme or slowing processing

Found some articles discussing this and phenytoin increases the liver toxicity of Tylenol.

Phenytoin induces the p450 enzymes CYP3A4 and CYP2C but not CYP2E1 or CYP1A2. Like carbamazepine, the
induction of CYP3A4 by phenytoin may lead to increased production of NAPQI from APAP.

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21
Q
  1. EKG of WPW (Wolf-Parkinson-White
A

A delta wave is slurring of the upstroke of the QRS complex b/c the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.

The combination of WPW and atrial fibrillation can potentially be fatal, especially if AV blocking agents are given (remember “ABCD” for adenosine, amiodarone, beta-blockers, calcium channel blockers and digoxin).
The medical treatment = procainamide (sodium channel blocker, Class I-A antiarrhythmic drug).

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22
Q

Which medication should you not use in WPW

A

DO NOT USE adenosine in WPW. It has been proven to cause VFIB. By blocking the AV node the extra electric pathway can go nuts. Also, the delta wave slurring can be on the front or back part of the QRS complex. Talked with multiple people, including anesthesiologists about this.

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23
Q

Wolff-Parkinson-White

What is it, what symptoms, and what treatment.

A

A syndrome in which an extra electrical pathway in the heart causes a rapid heartbeat.
The extra electrical pathway in Wolff-Parkinson-White syndrome appears between the heart’s upper and lower chambers and is present at birth.
Symptoms most often appear between the ages of 11 and 50 and include a rapid pounding heartbeat, dizziness, and lightheadedness.
Treatment may involve the use of medications or a procedure known as ablation. In rare instances, an electric shock may be used to restore a normal rhythm.

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24
Q
A

Wolfe Parkinson White Syndrome

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25
Q

The medical treatment for WPW syndrome

A

procainamide (sodium channel blocker, Class I-A antiarrhythmic drug).

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26
Q
  1. Methemoglobinemia question, what is it, answer OXIDIZED Fe3+ (causes L shift of HgB affinity)
A

Elevated levels of methemoglobin in the blood.
Methemoglobin is a form of Hgb that contains the ferric form of iron, whose affinity for oxygen is impaired. The binding of oxygen to methemoglobin results in an increased affinity for oxygen in the remaining heme sites that are in ferrous state within the same tetrameric hemoglobin unit. This leads to an overall reduced ability of RBC to release oxygen to tissues, with the associated oxygen–hemoglobin dissociation curve shifted to the left.
When methemoglobin concentration is elevated in red blood cells, tissue hypoxia may occur.

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27
Q

When methemoglobin concentration is elevated in red blood cells what occurs

A

associated oxygen–hemoglobin dissociation curve shifted to the left, tissue hypoxia may occur.

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28
Q

Pt received nitrous oxide for extractions and how has SOB, lethargy, ashen skin, palpitations, with tachycardia

9 cartridges of prilocaine and 2 cartridges of marcaine

What should you give him?

Diphenydramine
Nitroglycerine
Methylene Blue
Physostigmine

A

Large doses of priolocaine, greater than 600 mg can result in methmoglinemia in selected patients. Intravenous doses of articaine have been reported to cause similar problems. This occurs as a result of one of the metabolites of the drug converting reduced hemoglobin to methemoglobin. The patient will experience cyanosis with dark blood. Pulse oximetry remains normal since the monitor mistakenly interprets methemoglobin as oxyhemoglobin bu the actual oxygen carrying capacity is decreased resulting in th cyanosis. Small doses of methylene blue will convert the methemoglobin back to reduced hemoglobin.

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29
Q
A

Answer is methylene blue administration of 1 mg/kg IV

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30
Q
  1. Why do anesthetic gases work faster for peds pts?
A

Higher alveolar ventilation (and lower FRC).

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31
Q
  1. Why do gases work faster for peds pts

(8 pts)

A
  • Higher ratio of MV to FRC (FRC is low thus gas concentrations rise quickly)
  • Lower blood:gas partition coefficient in infants Cardiovascular
  • Greater cardiac output which goes to vessel-rich organs
  • Pediatric intravascular and extracellular fluid compartments are relatively larger than adults
  • Hepatic biotransformation pathways are immature in neonates and young infants
  • Protein binding is decreased
  • Metabolic rate is higher than adults
  • Infants have proportionately higher total body water than adults (70-75% vs. 50-60%) secondary to relatively higher fat content and smaller muscle mass
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32
Q

A few reminders about infants when considering pharmacology.

5 points

A

: 1) pediatric intravascular and extracellular fluid compartments are relatively larger than adults 2) hepatic biotransformation pathways are immature in neonates and young infants 3) protein binding is decreased 4) metabolic rate is higher than adults 5) infants have proportionately higher total body water than adults (70-75% vs. 50-60%) secondary to relatively higher fat content and smaller muscle mass.

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33
Q

Compared to adults, what do infants hav min terms of alveolar ventilation and FRC?

A

. This higher minute ventilation-to-FRC ratio along with higher blood flow to vessel rich organs leads to rapid rise in alveolar concentration, speeding induction. MAC requirements are highest at six months (except for sevoflurane, which are highest at birth and decrease at all age groups). This is why Neonatal Uptake is Faster (Barash).

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34
Q
  1. Ketamine IM dose Peds?
A

= Sedation/analgesia, 4-5 mg/kg as a single dose; may repeat dose (2-5mg/kg) if sedation inadequate after 5-10 mins or if additional doses are required
IV sedation dose: 1-2mg/kg over 30-60 secs
Induction IM dose 5-10mg/kg;
6.5-13mg/kg for >16YO
Induction IV dose 1-3mg/kg; 1-4.5mg/kg for >16YO

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35
Q
  1. Zofran MOA
A

selective 5-HT3 (serotonin) receptor antagonist

blocks serotonin, both peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone (in the area postrema of the medulla oblongata, which is located on the floor of the 4th ventricle and therefore outside the BBB).

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36
Q
  1. Parkinson’s disease, what drugs should you avoid.
    DM in the pM
A
  • droperidol, metoclopromide, prochlorperazine methotrimeprazine,
  • avoid dopamine receptor antagonists as they may cause extramidal symptoms to include: akathisia, parkinsonism, and tardive dyskinesia. Can treat with benadryl (OMSITE).
  • Dopamine depletion in the substantia nigra of the basal ganglia.
  • Lewy bodies (cytoplastmic inclusions).
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37
Q

Parkinson’s disease

(4 main points)

A

1-Characterized as an idiopathic movement disorder with akinesia, ‘resting pill’ rolling tremor and a shuffling gait.
2-Primary pathogenesis is dopamine depletion in the substantial nigra of the basal ganglia.
3-Lewy bodies (cytoplasmic inclusions) can be seen in Parkinson’s disease however are localized in the cerebellum, basal ganglia, sympathetic ganglion and spinal cord
4-Nothing seen in temporoparietal lobe

Leading cause of neurologic disease in people older than 65 years old and affects 1 million Americans. It is characterized as an idiopathic movement disorder with akinesia, ‘resting pill’ rolling tremor and a shuffling gait. The primary pathogenesis is dopamine depletion in the substantial nigra of the basal ganglia. Lewy bodies (cytoplasmic inclusions) can be seen in Parkinson’s disease however are localized in the cerebellum, basal ganglia, sympathetic ganglion and spinal cord and not usually the temporoparietal lobe.

Focal areas of demyelination followed by reactive gloss is seen in MS.

Myasthenia gravis is an autoimmune disease causing muscular weakness form antibody mediated destruction of the acetylcholine receptor in the neuromuscular junction. Weakness is temporarily ameliorated by the admin of edrophonium and that is a diagnostic for the disease.

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38
Q
A

c. Dopamine depletion in the substantiated nigra of the basal ganglia.

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39
Q
A

d. Pehnothiazines

These drugs block dopamine receptors and can lead to movement disorder and TMJ dislocation

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40
Q
A

C. levodopa should be discontinued 24 hrs prior to neuromuscular blocking agent

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41
Q
  1. Drug that can cause hypertension thereby counteracting the effects of hypertensive meds? =
A

= Ibuprofen

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42
Q
  1. Best vagal maneuver for kids?
A

= Put cold ice on face (vagal response- mammalian dive reflex).
In infants and young children (who can’t cooperate) apply a bag filled with ice and cold water to their face (the whole face) for 15-30 seconds. This will initiate the “diving reflex” whereby the child’s glottis closes, intrathoracic pressure increases and they valsalva.

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43
Q
  1. EtCO2 7mmHG during chest compression, what is the cause?
A

Inadequate CPR

High quality chest compressions are achieved when the ETCO2 value is at least 10-20 mmHg. When ROSC occurs, There will be a significant increase in the ETCO2. (35-45 mmHg) This increase represents a drastic improvement in blood flow (more CO2 being dumped in the lungs by the circulation) which indicates circulation.

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44
Q
  1. How do you treat a wide complex monomorphic tachycardia in a kid who is unstable? =
A

= Synchronized cardioversion 0.5-1 J/kg, bump it up to 2 J/kg if not effective (PALS)

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45
Q
  1. Succinylcholine in kids causes what cardiovascular symptoms
A

Bradycardia

The initial metabolite of succinylcholine, succinylmonocholine, produces a transient negative chronotropic effect through its stimulation of sinus node muscarinic receptors. Repeated dosing or infusions of SCh may lead to bradycardia that is appropriately treated with atropine.

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46
Q
  1. Upslope of EtCO2 curve?
A

Obstruction, new question said how do you tx, answer maybe suction?

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47
Q

Review how to treat pediatric tachycardia with a pulse and poor perfusion algorithm

A
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48
Q
  1. Max dose dantrolene?
A

10mg/kg

Treatment of MH = dantrolene 2.5 mg/kg IV, with subsequent bolus doses of 1 mg/kg IV until the signs of acute MH have abated. Rapidly via large-bore IV line, if possible, d/t the propensity of dantrolene to cause venous thrombi.

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49
Q

Contraindication to LMA?

A

None of the older below answers were there, possible answers were abnormal lung compliance vs emergency resuscitation

These are confirmed possibilities
oor pulmonary compliance, high airway resistance, pharyngeal pathology, risk for aspiration, and/or airway obstruction below the larynx

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50
Q

Absolute contraindication to LMA

A

trismus and complete upper airway obstruction

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51
Q

Relative contraindications to LMA

(8 pts)

A
  • Relative: increased risk of aspiration (morbid obesity, pregnancy >14 weeks of gestation, pt who is not NPO, upper GI bleed), abnormalities in supraglottic anatomy, need for high airway pressure >20mm H2O)
  • Potential pharyngeal/laryngeal pathology, poor pulmonary compliance, high airway resistance
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52
Q
  1. Hypertrophic Obstructive Cardiomyopathy (HOCM) anesthetic considerations
A

directed towards minimizing LVOT (Left ventricular outflow tract) obstruction by decreasing myocardial contractility and increasing preload and afterload

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53
Q

Events that decrease outflow tract obstruction

(10 pts)

A
  • Decreased myocardial contractility
  • B-adrenergic blockade
  • Volatile anesthetics
  • Calcium entry blocker
  • Increased/maintain preload
  • Hypervolemia (IV fluids)
  • Bradycardia (to allow ventricular filling)
  • Increased/maintain afterload
  • Hypertension
  • A-adrenergic stimulation

HCM-Hypertrophic cardiomyopathy
HOCM-Hypertrophic obstructive cardiomyopathy

Be careful with the table to the side as HCM and HOCM are two very different entities. HCM develops typically from hypertension. HOCM is a genetic condition bulging of the interventricular septum into the left ventricle where is blocks the outflow of blood. HOCM patients you want as normal as possible, maintain volume status, both pre and afterload, and normal HR. if you drop any of these the bulging gets worse and the cardiac output can tank.

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54
Q
  1. Erythromycin and versed
A

same enzyme so slower to process

Metabolism of both erythromycin and midazolam by the same cytochrome P450IIIA (CYP3A) isozyme may explain the observed pharmacokinetic interaction. Prescription of midazolam for patients receiving erythromycin should be avoided or the dose of midazolam should be reduced by 50% to 75%.

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55
Q
  1. Dexmedetomidine MOA? =
A

Also known as Precedex

Central a2 agonist.

(Reversal is atipamezole = synthetic a2 antagonist)

Alpha 2 agonists inhibit norepinephrine, acetylcholine, and insulin

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56
Q
  1. Treatment of symptomatic bradycardia in peds?
A

Start CPR if HR <60BMP.
If bradycardia persists:
IV/IO Epinephrine 0.01mg/kg of 1:10,000 (0.1mL/kg) q3-5min, Or ET Epi 0.1mg/kg of 1:1,000 (0.1mL/kg),
Or IV/IO Atropine 0.02mg/kg,
Or consider transthoracic/transvenous pacing.

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57
Q
  1. Damage of lingual nerve causes loss of?
A

Fungiform papilla

The persistence of fungiform papillae atrophy is an important severity indicator of the nerve injury, usually improves slowly during the first 6 months postoperatively. The lack of recovery in this period of time or duration of symptoms beyond 2 years is a sign of a bad prognosis and it makes unlikely a spontaneous somatosensory recovery.

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58
Q
  1. What does lateral pharyngeal space abscess present as
A

here was a question about this and how it could show as horners syndrome due to sympathetic block from abscess near sympathetic cervical chain

Horner’s: miosis, ptosis, anhidrosis. Blockage of sympathetic nerves to head and neck. The answer to this question is lateral pharyngeal space NOT retro.

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59
Q
  1. Where to I&D for masticator space? =
A

just inferior and parallel to angle of mandible

Masticator Space = confluence of: submasseteric, pterygomandibular, superficial temporal and deep temporal space.

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60
Q
  1. Acute hepatotoxicity with Tylenol and what other drug?
A

Statin,

The prescription agents known for their hepatotoxic tendencies include antiepileptic drugs, such as phenobarbital, phenytoin, and carbamazepine, as well as anti-tuberculosis drugs, such as isoniazid and rifampin. OTC herbs and dietary supplements such as St. John’s wort, garlic and germander, may mechanistically enhance the CYP system.
Although statins are the most publicized lipid-lowering medication in the arena of drug-induced liver injury, their potential to cause clinically significant liver injury is quite minimal. Sustained-release niacin is the only drug in this category that causes clinically significant hepatotoxicity.

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61
Q
  1. What is substance P? q what does it actually do
A

VASODILATOR

Substance P functions in the CNS as a neurotransmitter (neuropeptide), and its neurokinin (NK) receptor 1 are localized in distinct areas of the brain important in affecting behavior and the neurochemical response to both psychological and somatic stress.
Substance P is involved in sensory and nociceptive pathways. In the periphery, substance P has been identified in C-type sensory nerve endings and autonomic afferents throughout the body. Substance P is present at sites of inflammation, and inflammation can enhance its expression

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62
Q
  1. Symptoms of superior orbital fissure syndrome?

(5 pts)

A

mydriasis via CN3

a. Pupillary dilation via alteration in CN3 function in its innervation of the pupillary constrictors
b. Paresis of CN3, CN4, CN6 causing ophthalmoplegia
c. CN3 involvement = paresis of Levator palpebrae superiorus muscle = leads to ptosis (loss of sympathetic tone to Muller’s muscle since terminal sympathetic fibers travel with CNV1) + loss of superior palpebral fold.
d. Neurosensory disturbance to CNV1 with hypoesthesia/anesthesia of the supraorbital and supratrochlear nerves and loss of corneal reflex (afferent CNV1 nasociliary, efferent CN7 temporal and zygomatic).
e. Proptosis from engorgement of the ophthalmic veins and lymphatics.

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63
Q

What is ophthalmoplegia?

A

Ophthalmoplegia is the paralysis or weakness of the eye muscles. It can affect one or more of the six muscles that hold the eye in place and control its movement. There are two types of ophthalmoplegia: chronic progressive external ophthalmoplegia and internal ophthalmoplegia.

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64
Q

Orbital apex syndrome

(5 symptoms +1)

A

a. Pupillary dilation via alteration in CN3 function in its innervation of the pupillary constrictors
b. Paresis of CN3, CN4, CN6 causing ophthalmoplegia
c. CN3 involvement = paresis of Levator palpebrae superiorus muscle = leads to ptosis (loss of sympathetic tone to Muller’s muscle since terminal sympathetic fibers travel with CNV1) + loss of superior palpebral fold.
d. Neurosensory disturbance to CNV1 with hypoesthesia/anesthesia of the supraorbital and supratrochlear nerves and loss of corneal reflex (afferent CNV1 nasociliary, efferent CN7 temporal and zygomatic).
e. Proptosis from engorgement of the ophthalmic veins and lymphatics.
Orbital apex syndrome = all of the above + optic nerve (CN2) involvement = leads to changes in visual acuity.

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65
Q
  1. Adenosine MOA?

7 pts

A

= PURINE nucleoside
-acts at A1 and A3 receptors
-Dilates coronary vessels
-Increases myocardial contractility
-Depresses both SA AV nodes
-Dilates in healthy heart tissue, coronary steal in areas of occlusion with vasocontrstion after the occlusion
-may induce chest pain

A ubiquitous endogenous purine nucleoside, adenosine is primarily useful in cardiology. It also has neuromodulatory effects at the presynaptic receptor32 and in the spinal cord33 via the A1 and A3 receptors, which downregulate cyclic adenosine monophosphate (cAMP) through inhibitory G protein

adenosine binds to type 1 (A1) receptors

Adenosine is known to regulate myocardial and coronary circulatory functions. Adenosine not only dilates coronary vessels, but attenuates beta-adrenergic receptor-mediated increases in myocardial contractility and depresses both sinoatrial and atrioventricular node activities.

= Transient heart block at the atrioventricular (AV) node
-endothelial relaxation of smooth muscles as is found inside the artery walls
-Adenosine reduces blood flow to coronary arteries past the occlusion.

The administration of adenosine also reduces blood flow to coronary arteries past the occlusion. Other coronary arteries dilate when adenosine is administered while the segment past the occlusion is already maximally dilated, which is a process called coronary steal. This leads to less blood reaching the ischemic tissue, which in turn produces the characteristic chest pain.

This causes dilation of the “normal” segments of arteries, i.e. where the endothelium is not separated from the tunica media by atherosclerotic plaque.

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66
Q
  1. What causes V/Q mismatch leading to hypoxemia?
A

ARDS

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67
Q
  1. What is point at which elastic recoil of chest and lung are equal?
A

Functional Residual Capacity (FRC) is the volume of air present in the lungs at the end of passive expiration. At FRC, the opposing elastic recoil forces of the lungs and chest wall are in equilibrium and there is no exertion by the diaphragm or other respiratory muscles.

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68
Q

V/Q mismatch causes (7)

A
  • COPD
  • Asthma
  • Pneumonia
  • Chronic bronchitis
  • Pulmonary edema
  • Pulmonary Embolism
  • Airway obstruction: anaphylaxis, vocal cord inflammation, trauma or injury to the airway, smoke inhalation, swelling of the throat, tonsils, or tongue
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69
Q
  1. What is volume of distribution dependent on?
A

Answer LIPID SOLUBILITY, Jay went with concentration…
a. Lipid solubility, Non-ionizing drugs, lack of serum protein binding all have high volume of distribution

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70
Q
  1. What do halogenated anesthetics do to lung?
A

bronchodilator

Halogenated anesthetics include desflurane, isoflurane, sevoflurane

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71
Q
  1. What determines slow onset of bupivacaine?
A

Disassociation constant
a. Onset = pKa, duration of action = protein binding, potency = lipid solubility

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72
Q
  1. What type of impaction is easiest for coronectomy?
A

VERTICAL

Easiest? What kind of a question is that?
Works best for Vertical? Works worst for mesioangular.
Majority of coronectomy cases are vertical or mesioangular according to Peterson + Miloro

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73
Q
  1. What type of impaction likely to dislodge root in coronectomy?
A

Distoangular has higher root migration risk
Coronectomy is contraindicated (relative) in horizontal imp d/t increased risk of nerve injury with sectioning (Pogrel).

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74
Q
  1. Proptosis, periorbital edema after extraction #1
A

Postseptal/Retroseptal cellulitis (key is proptosis)

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75
Q
  1. Signs of Cavernous Sinus Thrombosis?
A

pain, proptosis, lid ptosis, high fever, CN6 palsy is most common nerve palsy (no abduction), CN3,4,6 palsy (ophthalmoplegia)- can be septic or aseptic, can also get paresthesia to CN V

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76
Q
  1. What is true of tooth fracture: apical 1/3 most common?
A

Ellis III most common? Splint for 2 wks?———

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77
Q

How Ong do root fractures need to be splinted for?

A

6 weeks

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78
Q

Ellis Classifications

A
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79
Q
  1. Goode ratio?
A

if nasofrontal angle 36-40 then nasal projection should be 0.55-0.60 of nasal dorsum length

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80
Q
  1. Wallace rule of 9’s
    how much surface area burned if head, one upper extremity and anterior torso burned
A

——- head-9, upper ext 9, torso to include chest and abd 18. (For reference lower ext is 18%)

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81
Q

Type 3 necrotizing fasciitis?

A

gas gangrene, eg due to clostridium

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82
Q

Types of necrotizing fasciitis

A

Type I (polymicrobial i.e. more than one bacteria involved)
Type II (due to haemolytic group A streptococcus, staphylococci including methicillin resistant strains/MRSA) Type III (based on marine speices and kind of a grab bag of other bacteria including clostridum) Type IV (fungal)

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83
Q
  1. Cleft palate with chr 22 deletion?
A

VCF (Velocardiofacial, also DiGeorge).

CATCH-22 (Cardiac anomalies, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia).

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84
Q
  1. Transcaruncular approach to medial orbital wall, what are anatomic landmarks?
A

caruncle + semilunar fold.

Incision posterior/lateral to caruncle and anterior/medial to semilunar fold (plica semilunaris).

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85
Q
  1. What type of flap is buccal fat pad?
A

Axial pattern based on terminal branches of IMAX

An axial pattern flap is a pedicle graft that incorporates a direct cutaneous artery and vein into its base.

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86
Q
  1. What is a random pattern flap?
A

No named blood vessel

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87
Q
  1. GCS scale, question was you were given the actual numbers and had to say mild, MODERATE, severe
A

Head Injury Classification:
Severe Head Injury—-GCS score of 8 or less
Moderate Head Injury—-GCS score of 9 to 12
Mild Head Injury—-GCS score of 13 to 15

CONFIRMED

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88
Q
  1. Bite wound closure and irrigation?
A

High pressure irrigation- at least 7psi, prophylactic abx for pasteurella
(canis from dog, multocida from cats), augmentin, e corrodens and staph from humans. 1L sterile saline.

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89
Q
  1. Hyphema:
A

What increase risk of rebleed? Answer was if its STAGE 3 or 4

Grade 1, <1/3 chamber
Grade 2 is 1/3 – ½
Grade 3 is ½ and up,
Grade 4 is total

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90
Q
  1. Hyphema: What increase risk of rebleed?
A

= Stage of hyphema = 50% is increased risk of rebleed.
- Use of ASA or ibuprofen, HTN, increased IOP, African American and hypotony.

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91
Q
  • AS above, listed factors for risk of re-bleeding for a hyphema are
A
  • hypotony (IOP of 5 mmHg or less)
  • elevated IOP,
  • 50% greater hyphema,
  • HTN,
  • African American
  • ASA use
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92
Q

Wat’s the first sign of traumatic optic neuropathy?

A

Relative Afferent Pupillary Defect
- Decreased visual acuity,
- loss of color differentiation (red)
- afferent pupillary defect

Relative Afferent Pupillary Defect (RAPD) is a condition in which pupils respond differently to light stimuli shone in one eye at a time due to unilateral or asymmetrical disease of the retina or optic nerve

Traumatic Optic Neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. T

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93
Q
  1. How much height needed from ridge for implant supported partial denture?
A

11mm

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94
Q
  1. What’s most stable reconstruction for multiple teeth missing
A

Implant supported FIXED partial?

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95
Q
  1. Loading force for zygomatic implant and anterior implant
A

40Ncm

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96
Q
  1. Tension vs compression zones of mandible?
A

q tension angle fx where? Answer Alveolus and external oblique ridge

Angle fracture = tension at ridge and compression at inferior border.
Anterior mandible fracture = opposite - compression at ridge and tension at inferior border.

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97
Q
  1. Least likely injury to nasolacrimal duct?
A

Bilateral superior orbital rim fracture? Anterior table comminution? Anterior and posterior table comminution?

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98
Q
  1. Osteochondroma tumor growth is by what mechanism?
A

Lichtenstein theory –

osteochondroma develops by the metaplastic changes in the periosteum, as the pluripotent periosteum has the potential to differentiate into osteoblasts and chondroblasts.

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99
Q
  1. Most common odontogenic tumor?
A

Odontoma > Amelo

benign most common odontogenic tumor

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100
Q
  1. CN3 palsy will cause what? Answer DOWN and OUT eyes
A

(Only CN4 and CN6 are working, resulting in downward and lateral gaze, along with fixed dilated pupil).

Remember CN IV is superior oblique and VI is the abducens leading to

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101
Q
  1. Best method for canalicular repair?
A

Crawford 3-4 MONTHS
= Crawford silastic tube/stent, at least 12-16 weeks (3 mos) in adults (shorter for peds – 8-12 weeks). See OMSITE question.

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102
Q

How long after inferior canaliculus laceration repair and intubation should the stent remain in place in the adult pt?
A) 1-2 weeks, B) 4-6 weeks, C) 7-10 weeks, D) 12-16 weeks

A

Rationale: Inferior canaliculus injuries need repair within 24-48 hours in order to prevent epiphora. Repair of this kind of injuries is usually carried out by loop intubation with the punctate being initially cannulated with silastic stents. The stents extend from the puncta through the nasolacrimal duct and emerge in the inferior meatus, and should remain in place for at least 3 months in the adult. In cases of pediatric injuries, the same procedure is performed; however, the stent can be removed in a shorter amount of time.

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103
Q

Tests for latency of the nasolacrimal duct

A

. Jones 1 test is similar to a DDT, dye disappearance test. Put fluorescein into the fornix of each eye and see if moves thru the nasolacrimal system, check inside in the nose at 2 minutes and 5 minutes, this checks the system under normal physiologic conditions. Jones 2 is non-physiologic, you inject the mixture into the system to see if it comes out the nose after a Jones 1 test is negative.

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104
Q
  1. Class III malocclusion requiring maxillary advancement and downgrafting—why relapse after one year?
A

= Least stable move is the downgraft- likely relapse is due to maxilla going up in 1 yr post op
This answer is do to ortodontic tipping of teeth in some way, very poorly worded (never actually said “tipping”)

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105
Q
  1. Crouzon syndrome – what happens to mandible growth?
A

UNCHANGED
= Mandible growth should remain unaffected

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106
Q
  1. Indications for uses of oral appliance
A

= Primary snoring and mild OSA

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107
Q
  1. Patient with OSA from hypopharynx obstruction, SNA 79 SNB 76 what is best treatment
A

MMA

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108
Q
  1. Where do maxillary and mandibular bone come from
A

Branchial arch 1, mesoderm

Test said ectoderm, but we are sure it is mesoderm

ectoderm

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109
Q
  1. Palatoplasty most maxillary growth restriction?
A

Wardill-Kilner V-Y pushback

Scarring of the hard palatal tissues is associated with maxillary growth inhibition. Techniques that minimize the degree of palatal scarring are considered beneficial to overall maxillary growth. The pushback palatoplasties leave areas of the anterior hard palate denuded to heal by secondary intention with resultant scarring. Multiple studies have reported greater growth impairment secondary to these techniques versus the von Langenbeck palatoplasty, with some centers abandoning the push-back for that reason.

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110
Q
  1. Clover leaf deformity, Kleeblattschadel?
A

Hydrocephalus. (I think ans. was the single word HYDROCEPHALUS) Pfeiffer type 2

Kleeblattschadel Skull, or clover lead deformity, is a very rare cranial pansynostosis which affects the entire calvarium making it look like a tri-lobed clover leaf (the face being the 4th leaf). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4337142/

Pfeiffer Type 2 is a bunch of abnormalities and clover leaf skull

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111
Q
  1. soft tissue change ratio for chin alloplastic implant? =
A

0.8 to 1.0 hard to soft tissue movement

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112
Q
  1. lingual frenectomy? How often needed in infants? Changes in latching? Does type of frenectomy affect outcome?
    ??
A

ans outcomes do not depend on technique

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113
Q
  1. High mandibular plane angle and low hyoid causes what
A

Poor outcome for cosmetic surgery?

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114
Q
  1. Lower lid retraction? What is distance and time (in sec) that is normal
A

Peterson says: Snap and distraction 7mm/1sec
Old OMSITE says Snap 1-3secs, and distraction <6mms normal

6mm and 1second

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115
Q
  1. Tip of nose innervation?
A

External branch of anterior ethmoid nerve (CNV1).

Can also be innervated by infratrochlear, supratrochlear, and infraorbital.

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116
Q
  1. Trichophytic brow lift indications in what types of patients? =
A

= Long forehead, thinning hair in temporoparietal areas.
Will decrease brow height/lower hair line. Can improve hair thinning in TP areas by excising areas of hair loss.

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117
Q
  1. Keystone area?
A

NASAL BONES and upper lateral cartilage

The keystone region consists of contributions from the paired nasal bones cephalically, paired upper lateral cartilages (ULCs) caudally, quadrangular cartilage anterior-inferiorly, and perpendicular plate of the ethmoid (PPE) posterior-inferiorly.
= confluence of nasal bone and cartilage at the junction of the upper and middle thirds of the nose.
Its importance to the stability and structure of the nose is exemplified by the number of complications that may arise from poor surgical handling of this area.

More simply, it is where the ULCs meet the nasal bones, as opposed to the scroll which is where the ULCs meet the LLCs

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118
Q
  1. Keystone area? NASAL BONES and upper lateral cartilage
A

The keystone region consists of contributions from the paired nasal bones cephalically, paired upper lateral cartilages (ULCs) caudally, quadrangular cartilage anterior-inferiorly, and perpendicular plate of the ethmoid (PPE) posterior-inferiorly.
= confluence of nasal bone and cartilage at the junction of the upper and middle thirds of the nose.
Its importance to the stability and structure of the nose is exemplified by the number of complications that may arise from poor surgical handling of this area.

More simply, it is where the ULCs meet the nasal bones, as opposed to the scroll which is where the ULCs meet the LLCs

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119
Q
  1. How does the ULC and LLC joint at the scroll?
A

Answer interlocking

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120
Q
  1. Most common complication of alloderm:
A

? Assuming infection. But can’t

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121
Q

Nasal Anatomy

A
122
Q
  1. Medium chemical peel through what layer?
A

Upper reticular dermis
The upper reticular dermis is penetrated by medium depth peeling agents (TCA 30-50%, Jessner’s plus 30 %TCA, 88% Phenol) and the mid-reticular dermis is penetrated by deep peeling agents like Baker’s phenol and Litton’s phenol). OMSITE 2008

123
Q
  1. MRI with ADD without reduction= TMJ classification
A

= Wilkes 3

124
Q
  1. Histology of a forehead lesion with keratin pearls
A

Most likely SCC

125
Q
  1. Best reconstruction for a 1cm forehead defect
A

Local advancement / rotational flap

Showed a pic of a guy with a oval black WordArt circle thing over his left eye mid forehead
Advancement is the most common design of flaps used for forehead reconstruction. Among the main benefits of advancement flaps are maintaining a natural contour of the forehead, facilitating optimal scar placement in horizontal forehead creases, and usually providing an adequate source of skin for reconstruction. Multiple designs for advancement flaps are possible, including unilateral, bilateral, subcutaneous tissue pedicle, and A-T and O-T repairs. Bilateral advancement flaps often take the form of an H-plasty if two parallel incisions are made to create the flaps. If single incisions are used, repair assumes the form of a T-plasty (see discussion in Chapter 6 Bakers Forehead flaps)

126
Q
  1. TMJ osteoarthritis, presence of what is characteristic?
A

GAG, protein, IgG
The results suggest that IL-1β levels in synovial fluid of the TMJ have a positive correlation with OA change. The MMP3 activity detected was greatly increased in patients with cartilage degradation. These findings suggest that both changes may be important markers of early bone deterioration in TMJs that are undetectable by radiograph imaging.
The key mediators of cartilage degradation include the matrix metalloproteinases (MMPs) and the closely related aggrecanases. Collagen type II is degraded by the first, while aggrecan, the major proteoglycan in cartilage, is degraded by both. These proteases, especially aggrecanase-1 and -2, are important mediators of aggrecan loss in cytokine-stimulated normal cartilage and in already-damaged OA cartilage. MMP-1, -3 and -9 are abundantly present in cartilage and synovial fluid in joints under pathologic conditions

127
Q
  1. What fat graft after parotidectomy?
A

Prevent AURICULOTEMPORAL syndrome?

Prevent Frey (auriculotemporal) Syndrome = aberrant regeneration of post-ganglionic parasympathetic fibers (from ATN CNV3) to postganglionic sympathetic fibers that innervate the sweat glands of the face.
Dermis-fat grafts were performed on 7 patients at the time of parotidectomy to prevent Frey’s syndrome and the characteristic concave deformity. Only 1 patient demonstrated postoperative Frey’s syndrome, and 1 demonstrated a slightly concave deformity due to fat absorption. Although other barrier materials have been reported to achieve success in preventing gustatory sweating, our method simultaneously corrects the associated deformity of facial contour as well. (Dermis-fat graft after parotidectomy to prevent ‘Frey’s syndrome and the concave deformity’

128
Q
  1. Patient s/p TMJ replacement still with pain, why?
A

Neuropathic pain?

129
Q
  1. Patient s/p TMJ replacement still with pain, why?

(Intrisic - 9)
(Extrinsic- 9 )

A

Intrinsic etiologies:
Infection, Heterotopic bone formation, Dislocation, Material sensitivity, Aseptic component or screw loosentin, Component or screw fracture, Osteolysis, Neuroma formation, Synovial entrapment syndrome

Extrinsic etiology:
Prior misdiagnosis, chronic centrally mediated pain, persistent myofascial pain, Neurologic injury, Complex regional pain synd, Temporalis tendonitis, Coronoid impingement, Freys neuralgia, integrin formation

130
Q
  1. Why use TCA for TMJ pt?

(4 things)

A

1-Pain relief by inhibiting pain signals and decreasing neuropathic pain
2-Bruxism control
3-Anti-axieity
4-Promotes good sleep

TCA = SNRI Serotonin-Norepi receptor inhibitor) – inhibits pain signals.
= Pain relief, bruxism control and sleeplessness (TCA induces analgesia at low doses w/o antidepressive effects) Decrease neuropathic pain (overall pain), anti-anxiety, act like muscle relaxants (reduce clenching and grinding), and promote good sleep.

Examples include
Amitriptyline.
Amoxapine.
Desipramine (Norpramin)
Doxepin.
Imipramine (Tofranil)
Nortriptyline (Pamelor)
Protriptyline.
Trimipramine

131
Q
  1. Alloplastic joint vs rib graft differences?
A

Ankyloses? Soft diet?
Rib graft: IMF is necessary to allow for initial consolidation of the graft (usu 4–6 weeks).
Rib will ankylose if prolonged IMF.
Alloplastic: early mobility with soft or nonchew diet

132
Q
  1. Most common complication of rib graft to reconstruct condyle?
A

Asymmetrical and unpredictable growth

  • TMJs reconstructed with costochondral grafts revealed that excessive growth on the treated side occurred in 54%of the 72 cases examined, and equal growth with the opposite side occurred in 38% of the cases.
  • Pneumothorax 4-30% of time
133
Q
  1. Painful joint from STD with fever, swelling, malaise
A

chlamydia or gonorrhea??? 50/50 (both were options)

If painful – reactive arthritis (Reiter’s syndrome: can’t climb, can’t see, can’t pee) = chlamydia and gonorrhea. If septic – septic arthritis (gonorrhea, syphilis)
- Chlamydia trachomatis - study by Drs. Hughs, Hudson and Wolford published in the Journal of Maxillofacial Surgery (2000) found the bacteria, associated with the sexually transmitted disease Chlamydia, were present in 65% of a TMJ surgery patient group.
- On a microbiological level, the pathogenesis of SATMJ involves hematogenous dissemination of causative microorganisms or direct extension of a contiguous infection, and the infection was often caused by bacteria including Staphylococcus aureus, Neisseria gonorrhea, Streptococcus and Aspergillus flavus.f

134
Q
  1. Photo of black person’s finger nail or tip of finger
A

Acral lentiginous melanoma

Acral lentiginous melanoma (ALM) is a specific type of melanoma that appears on the palms of the hands, the soles of the feet, or under the nails (Hutchinson sign = pigmentation under nails). Melanocytes contain your skin color (known as melanin or pigment). In this type of melanoma, the word “acral” refers to the occurrence of the melanoma on the palms or soles. The word “lentiginous” means that the spot of melanoma is much darker than the surrounding skin. It also has a sharp border between the dark skin and the lighter skin around it. This contrast in color is one of the most noticeable symptoms of this type of melanoma. Though relatively uncommon in the general population, ALM is the most common type of melanoma in people with darker skin and those of Asian descent. However, it can be seen in all skin types. ALM may be hard to recognize at first when the patch of darkened skin is small and looks like little more than a stain or bruise. ALM sometimes develops from an existing mole. It can also occur seemingly out of nowhere on healthy skin. Early diagnosis and treatment are essential.

135
Q
  1. African vs American Burkitt’s lymphoma?
A

high-grade non-Hodgkin’s B cell lymphoma.
= Endemic/African = jaw, EBV-associated.
= Sporadic/American = ileocecal (pelvic/abdomen), abdominal pain. Starry sky appearance.

136
Q

ommon bacterial in chronic parotitis S. aureus (usu MRSA) vs Strep viridans

A

The adult form has been more closely associated with infection from S. aureus (usually MRSA), whereas Streptococcus viridans is the major pathogenic bacteria in the juvenile form

137
Q
  1. Rhabdomyosarcoma treatment rhabdo stages based on resection margin-
A

type 1 no residual- type 2 microscopic tumor, type 3 gross tumor left, type 4 Mets. Add actinomycin-d and radiation to stage 2-4

  • Type 1 = no residual tumor = tx: VAC (Vincristine, adriamycin, cyclophosphamide)
  • Type 2 = microscopic tumor left = tx: VAC + XRT (4,000-6,000 cGy over 6 weeks)
  • Type 3 = gross tumor left = tx: VACA (Actinomycin-D) + XRT (4,000-6,000 cGy over 6 weeks) to primary site and any metastatic focus.
  • Type 4 = metastases = tx: VACA (Actinomycin-D) + XRT (4,000-6,000 cGy over 6 weeks) to primary site and any metastatic focus.
  • Tumors of OMS areas, surgery does not include regional LN dissection. Cont chemo for 1 year, or if suspicion for residual disease, up to 2 years.
138
Q
  1. KCOT treatment (aka OKC):
A

all bad choices but they were resection only option, enucleation not a surgical option, no soft tissue invasion

139
Q
  1. What requires Large Resection margins (1-1.5cm):
A

CEOT, Myxoma, Ameloblastoma

140
Q
  1. How to treat ameloblastic fibro-odontoma?
A

enucleation and curretage

Peds tumor: simple enucleation is required but the only good answer was enucleation and curretage

CONFIRMED

141
Q

AFO RUN DOWN (AMELOBLASTIC FIBRO-ODONTOMA

A
  • The ameloblastic fibro-odontoma is defined as a tumor with the general features of an ameloblastic fibroma but that also contains enamel and dentin. Such lesions appear to be true neoplasms. Simple enucleation (Neville)
  • Marx: not a neoplasm, but, like the cementoblastoma and the odontoma, a hamartoma.
142
Q
  1. Chronic perio histology?
A

When soft tissue from areas of periodontitis is examined microscopically, gingivitis is present and the crevicular epithelium lining the pocket is hyperplastic, with extensive exocytosis of acute inflammatory cells. The adjacent connective tissue exhibits an increased vascularity and contains an inflammatory cellular infiltrate consisting predominantly of lymphocytes and plasma cells, but with a variable number of polymorphonuclear leukocytes. Frequently, large colonies of microorganisms, representing plaque and calculus, are noted.

143
Q
  1. Lichen planus characteristics: 7 comes to mind
A

6 characteristics

1-T-cell mediated sub-basilar split with lymphocytes, type IV cytotoxic (T-cell mediated) reaction, T8 lymphocytes attack basal cells that develop an unknown antigenicity,

2- FEMALES (2%), 40 y/o, Skin/mucosal lesions, Skin: pruritic scaly pink, vialoaceous/pigmented rhomboid plaques on flexor surfaces of wrists and ankles, Crisscrossed by Wickham striae

  1. Oral types- Reticular LP, Atrophic/Erosive LP
  2. Frequent on buccal mucosa, dorsal tongue, lateral tongue (high risk area, biopsy), gingiva, labial mucosa.
  3. Frequently infected with candida, White striae that don’t rub off
  4. . Positive Nikolsky sign (rarer)
  5. Histology- thin band of infiltrative lymphocytes, hugging contours of epithelium, NOT in the CT, Liquefaction of basal cells, EXOCYTOSIS – lymphocytes travel out to epithelium , Civatte bodies: dying basal cells look apoptotic, and necrotic, red in color, Saw tooth rete ridges
144
Q
  1. Homograft rejection is due to T cells
A

Rejection of solid organ allografts is the result of a complex series of interactions involving coordination between both the innate and adaptive immune system with T cells central to this process. The ability of recipient T cells to recognize donor-derived antigens, called allorecognition, initiates allograft rejection. Once recipient T cells become activated, they undergo clonal expansion, differentiate into effector cells, and migrate into the graft where they promote tissue destruction. In addition, CD4 T cells help B cells produce alloantibodies

145
Q
  1. Oral neurofibroma characteristics:
    8 types
A

-Most common peripheral nerve tumor
-stains for S100
-Arises from perineurial fibroblasts that incorporate Scwann cells & axons
-Skin, tongue, buccal mucosa asymptomatic
-Subtype: Dermal = no malignant transformation.
-Plexiform = malignant transformation, assoc with
-neurofibromatosis 1 (von Recklinghausen dx).
NF1 = café au lait spots (smooth “coast of California” border), Lisch nodules, optic pathway gliomas, Crowe sign.

146
Q
  1. Thyroglossal duct cyst excision?
A

take HYOID

Sistrunk procedure- take 1-2cm central hyoid bone with it

147
Q
  1. Desmoplastic fibroma

(10 characteristics)

A

rare central bone tumor- resection.

If near vital structures may use chemo and rads.
a. Locally aggressive benign myofibroblastic tumor of the jaws that occurs in patients younger than 30, mean of 14.
b. Equal gender,
c. mandible more common than maxilla.
d. Asymptomatic or painful swelling,
e. loose teeth, and/or
f. trismus.
g. Cortical perforation,
h. root resorption.
i. Radiographically, multilocular or unilocular radiolucency, well or ill-defined.
h. Extension into surrounding soft tissue not uncommon.

Treatment:
Curettage results in 30-90% recurrence.
c. Resection with 1-1.5cm bone margins

148
Q
  1. Trismus after radiation is due to what?
A

FIBROSIS

Radiation fibrosis within the masseter and medial pterygoid muscles OR
Restrictive fibrosis in the mucosa of the anterior tonsillar pillar and retromolar areas.

149
Q
  1. Safe pathologic margin for SCC?
A

5mm

= Clinical margins are generally about 1 to 1.5 cm. Although close surgical margins can contribute to local recurrence after resection in oral cancer.
- Pathological margins more meaningfully predict local recurrence than do clinical margins. Liao et al. reported that pathological margins of more than 7 mm decreased the local relapse rate significantly. In general, many authors recommend pathological margins greater than 5 mm.
- Close margins have been defined as 3 mm or less, 4 mm or less, and 1 mm to 4.9 mm. An adequate clear margin is thought to be more than 3 mm, more than 5 mm, or 7 mm. According to most authors, an adequate pathological margin is at least 5 mm. (Surgical margins for the extirpation of oral cancer JKAOMS).

150
Q
  1. Histo with giant cells?
A

photo looked like peripheral giant cell lesion ABC, CGCG, Cementoblastoma, Cherubism, Brown tumor of hyperparathyroidism Aneurysmal bone cyst =

Central giant cell lesion =

Cherusibm =

151
Q
  1. Acanthomatous ameloblastoma looks like what histologically?
A

Squamous Cell Carcinoma
(or Squamous odontogenic tumor)

When extensive squamous metaplasia, often associated with keratin formation, occurs in the central portions of the epithelial islands of a follicular ameloblastoma, the term acanthomatous ameloblastoma is sometimes applied. This change does not indicate a more aggressive course for the lesion; histopathologically, however, such a lesion may be confused with squamous cell carcinoma or squamous odontogenic tumor (Neville and Damm)

152
Q

Cisplatin mechanism of action is

A

Cisplatin is a chemotherapy medication used to treat a number of cancers.

interferes w/ dna cross-linking

The mechanism of action of cisplatin has been associated with ability to crosslink with the urine bases on the DNA to form DNA adducts, preventing repair of the DNA leading to DNA damage and subsequently induces apoptosis within cancer cells.

= Nausea, vomiting, low mag/K+/Ca2+, myelosuppression, ototoxicity, nephrotoxicity
a. The following side effects are common (occurring in greater than 30%) for patients taking Cisplatin:
Nausea and vomiting, Low blood counts, Kidney toxicity, Ototoxicity, Blood test abnormalities (low mag, low ca2+, low K)
b. These are less common side effects (occurring in 10-29%) for patients receiving Cisplatin:
Peripheral neuropathy, appetite loss, taste changes, metallic taste, Increases in liver function tests, Hair loss

153
Q

What chemotoxicities are associated with cisplatin?

A

ototoxicity
Nephrotoxicity

154
Q

Ossifying fibroma vs fibrous dysplasia, what separates teh two?

A

clinically evident encapsulation

= Resection, 5mm margins. (resection recommended if):
- Involvement of (or within 1 cm of) the inferior border
- Extension into the maxillary sinus or nasal cavities, and/or
- Loss of encapsulation radiographically or clinically resection margins need be no larger than 5 mm. (MARX)

155
Q
  1. STSG 0.03in - what are the complications
A

HAIR
STSG= 0.030in is thick
Thin 0.008-0.012in, Med 0.012-0.018in (0.30-0.45mm), Thick 0.018-0.030.
= Thicker STSG resembles FTSG = lower survival rates and slower healing.

156
Q
  1. FTSG how much dermis do you take? =
A

= Includes the epidermis and dermis (OMSITE 2009)

157
Q
  1. What is the most common nerve injury with AICBG?
A

Iliohypogastric

158
Q
  1. Tongue flap harvesting principles =
A

= Depth 5mm, 1/3-2/3 of width of tongue, can extend posteriorly to within 1cm of the circumvallate papilla and anteriorly to within 1cm of the tip of the tongue

159
Q
  1. Skin grafts around implants?
A

Contraindicated grows hair, OK but if skin reaction move implant, may be only adequate source of tissue in cancer patients……What is this question asking?
= I think the indication for STSG with implants will be to do simultaneous vestibuloplasty for implant overdentures. Not sure there’s a good indication to do it around the actual implant.

Also, in some situations, skin grafts are used to balance or thicken tissue around dental implants to allow a more natural symmetrical relationship with the ..

160
Q
  1. Blood supply of DeltoPectoral flap
A

Internal mammary artery

161
Q
  1. Timing of skin graft inosculation/neovascularization

skIIN Graft

A

a. Imbibition = 24-48 hours = oxygen and nutrition to graft is supplied by the underlying bed via plasmatic diffusion or imbibition.
b. Inosculation = 48-72 hours = linking up of the blood vessels between the graft and wound bed.
c. Neovascularization = >72 hours = formation of new blood vessels.

162
Q
  1. Why prepare donor site for bone graft?
A

Prepare the site by making small osteotomies to allow inflow of blood/inflammatory factors for integration/healing of graft. (anyone have a better answer?) - but this says donor site and not recipient site?
- RAP (regional acceleratory phenomenon) by creating perforations increases release of growth factors and BMP.

163
Q
  1. TAD failure due to
A

Peri-implant mucositis

164
Q
  1. Platform switching and crestal bone resorption
A

= Use of narrower restorative abutments on a wider implant body

= Decreases crestal bone resorption by preventing migration of epithelium past the implant-abut interface, enhancing the connective tissue-osseous attachment in the crestal area.

165
Q
  1. Height of bone to contact point to preserve papilla
A

= 5mm or less.

166
Q

in 75% of patients, in order for the dental papilla to fill the embrasure space of a single tooth dental implant supported restoration, the maximum distance between the crystal bone and teh contact point is

A

6 mm

167
Q
  1. Condylar hyperplasia diagnosed with scintigraphy
A

what is difference between the two condyles?

= Uptake differences of 10% or more between the left and right condyles, with increased uptake ipsilateral to the CH, are considered to be evidence of active growing CH.

a technique in which a scintillation counter or similar detector is used with a radioactive tracer to obtain an image of a bodily organ or a record of its functioning.

168
Q
  1. Difference in percentage between Frankfort horizontal and natural head position
A

= 4.63 (other sources say 1-5 degrees).
- 3-4% (depending on gender)

169
Q
  1. What determines failure of subepithelial connective tissue graft?
A

SIMULTANEOUS PLACEMENT
Pocket technique, open palatal harvest, immediate graft with implant placement vs delayed 8 wk to graft??
a. The subepithelial connective tissue graft can be used during initial implant-site development before implant placement or simultaneous with submerged implant placement for the correction of small-volume soft tissue aesthetic ridge defects. Similarly, the connective tissue graft can be performed simultaneously with an abutment connection or nonsubmerged implant placement to reconstruct these small-volume soft tissue defects or for the correction of soft tissue recession defects that develop in the recall period. Finally, whenever a huge-volume soft tissue aesthetic ridge defect is present, a series of connective tissue grafts is usually required for reconstruction of these aesthetic ridge defects before implant placement. (Peterson)

170
Q
  1. What is indication for subepithelial connective tissue graft
A

thin GLOSSY gingiva
can achieve up to 3mm, other answer said gain 5mm thickness which was WRONG

171
Q
A
172
Q
A
173
Q
A
174
Q
  1. When is PTFE indicated – horizontal vs vertical bone defect?
A

vertical

Polytetrafluoroethylene (PTFE) is a synthetic fluoropolymer of tetrafluoroethylene. Being hydrophobic, non-wetting, high density and resistant to high temperatures, PTFE is an incredibly versatile material with a wide variety of applications, though it’s perhaps best-known for its non-stick properties.

175
Q
  1. What has high rate of infection and movement – cranial autogenous graft, porous polyethylene, PTFE?
A

= PTFE would have higher rate of movement, but in terms of infection, could be porous polyethylene vs PTFE.
- PTFE has an extremely strong bond between carbon and fluorine for its nondegradable, biologically inert properties. There is no enzyme in the body capable of cleaving carbon-flourine bonds. The woven pattern of fibrils in the nonreinforced sheets, consisting of long chains of repeating units, allows the material to stretch in any dimension as well as to compress in thickness. Soft tissue on the outer surface consisted of soft tissue and keratinized tissue, the inner compartment had loose connective tissue with delicate collagen fibbers, which was well vascularized and number of vessels increased towards the bone surface. Studies also showed that the porosity of the PTFE membrane which was approximately 50 microm in diameter allowed invasion of cells and small blood vessels allowing the formation of thin collagen.

176
Q
  1. Polylactic acid vs collagen membrane differences
A

immune reaction (seen w/ PLA)

= Collagen membranes, b/c they have higher success rates. The releases of oligomers and acid byproducts during degradation of PLA may trigger inflammation reactions and foreign body response in vivo.

177
Q
  1. Best treatment for root prior to graft?
A

Tetracycline

178
Q
  1. Changes to keratinized gingiva when orthodontically erupting a nonrestorable anterior teeth: what happens to mucogingival junction and gingiva?
A

= Attached and keratinized gingiva thickened. MGJ does not move
Mucogingival junction should remain unchanged. Keratinized gingiva should increase, following the CEJ as the tooth is orthodontically erupted.

179
Q
  1. Treatment for brown recluse spider bite?
A

Dapsone
Self-limiting, does not have a specific treatment, but dapsone has been shown to assist in preventing tissue necrosis.

180
Q

What causes pulmonary HTN?

A

von-Euler- Liljestrand (hypoxic pulmonary vasoconstriction) mechanism allows for autoregulation of vascular bed in lungs for areas that are less well ventilated. This leads to small hypoxia environment and optimizes blood flow to areas that are well ventilated- good physiology

  • Right heart failure is usually a sequelae of pulmonary HTN.
  • OSA + pulm HTN- chronic hypoxia causing increase in HH cause blood to be more “viscous”- also the von-Euler- Liljestrand (hypoxic pulmonary vasoconstriction) mechanism allows for autoregulation of vascular bed in lungs for areas that are less well ventilated. This leads to small hypoxia environment and optimizes blood flow to areas that are well ventilated- good physiology- in OSA the whole lung is under ventilated so the mechanism kicks in throughout- rather than in small areas to optimize. This is called hypoxic pulmonary vasoconstriction -in OSA rather than optimizing VQ- the whole lung vasculature constricts causing pulm HTN.
  • Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure. Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised vasoconstriction of the pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to pulmonary hypertension.
181
Q
  1. Antibiotic treatment and dentoalveolar fracture in peds does it affect pulp survival?
A

YES IT HELPS
= Possibly, by decreasing risk of infection if dirty wound bed.

182
Q
  1. Juvenile osteoarthritis treatments:
A

steroid injection vs arthroscopic lysis and lavage?
- NSAIDs ease pain and reduce inflammation but do not prevent joint damage. Intra-articular corticosteroids offer a very rapid relief of symptoms and can spare the need for systemic therapy among patients with persistent oligoarticular arthritis. Intra-articular corticosteroids might be beneficial in cases where active TMJ arthritis persists despite a use of systemic therapy, and other joints remain in remission [72].
- There is evidence that intra-articular corticosteroid therapy (IACS) is effective in many patients with TMJ arthritis, and although its short-term safety profile has been well established, there remain concerns about long-term effects on mandibular growth

183
Q
  1. Arthrocentesis landmarks
A

tragal canthal line and distances Holmlund-Hellsing Line = Tragus to Lateral Canthus
a. 10mm anterior of mid-tragus and 2mm below the canthotragal line
b. 20mm anterior of mid-tragus and 10mm below the canthotragal line

184
Q
  1. Most common pediatric condylar fracture
A

Compression

185
Q
  1. Timing of GSW definitive surgery to minimize infection?
A

7-14 days
7-10 days to minimize infections, 10-14 day best overall consider infection and recon, and 21 days to prevent fibrosis so it depends on how exactly the question is asked. Most likely answer is 7-14 days, 21 days is really long, recon would be reallllyy hard

186
Q
  1. Where to wire tendon in ipsilateral NOE:
A

= Posterior superior direction (posterior lacrimal crest)
-But, other versions ask how to wire it which is contra-lateral, superior, see AO trauma for reference

187
Q

Stabilization of the medial cantal tendon during a medial cnathopexy should be direct at which of the following directions?

A

posterior and superior C

Repair of detached medial cnathal tendons during a severe nano-orbital ethmoidal fracture repair involves reattachment of one or both tendons to the posterior lacrimal crest in a slightly superior and superior direction to overcome the forces of migration, relapse and telecnathus

188
Q
  1. Horizontally unfavorable angle fracture causes by pull of what muscle?
A

Masseter

189
Q
  1. Cellular scaffolding graft:
A

promotes angiogenesis? Gets engrafted in recipient site?
Osteoconduction: acts as a matrix for bone growth.
These scaffolds are designed to be chemically biocompatible, biodegradable, and porous such that they promote vascularization, have sufficient mechanical strength and provide physical and biochemical stimuli.

190
Q

ow much of tooth apex opening is ideal if tooth is injured?

A

1 mm

191
Q
  1. How much does pulp regenerate
A

0.25mm/day

192
Q
  1. Why is zygomatic implant integrated
A

Engagement of four cortices. Other Q asks for torque, 40 NCMs

  • From a qualitative view, Nkenke et alindicated that the zygoma bone had poor trabecular bone density but a strong cortex, suggesting that primary stability of the zygoma fixture could be achieved if it is inserted in zygomatic cortical bone. Furthermore in a microcomputed tomography study, Kato and colleagues found that the trabecular bone at the end of the zygomatic fixture is thicker and wider than in other regions of the zygoma bone. These investigators suggested that after osseointegration, this thickening significantly assists the support of the zygoma fixture.
  • Ujigawa and colleagues compared functional stress distribution of zygoma implants with and without connected dental implants supporting a superstructure in a severely atrophic maxilla. These investigators found in the connected implant model that the stress was mostly concentrated in the zygoma bone and the middle of the implant. In contrast, the stress in the single implant model concentrated in zygoma bone, middle of the implant, maxillary alveolar bone and implant-abutment joint. These findings showed that a better distribution of forces occurs when all the implants are splinted with the prosthetic reconstruction. (Oral Maxillofacial Surg Clin N Am 25 (2013) 223–239)
  • Branemark found the zygoma to possess the quality of bone similar to the anterior mandible, which is widely known to have a high success rate of implant survival and to be of sufficient quantity.
  • Implant integration occurs within the thick bone in the body of the zygoma, which produces an integrated length in the range of 15-20mm. Acquisition of an additional zone of integration at the level of the alveolus is welcome, but unnecessary. The zygoma implants with a fully textured and threaded surface allows the potential for optimal integration anywhere along the buried implant shaft. (Current Therapy in Oral and Maxillofacial Surgery by Bagheri).
193
Q
  1. Stage of SCC if ipsilateral 1.5cm node?
A

Stage 3 (T? N1, assuming no mets).

194
Q
  1. Adjuvant treatment (chemoRT) indicated in what cases of SCC?

(6 pts)

A
  • extracapsular spread, +/- positive margins
  • Adjuvant XRT = T3 or T4 primary,
  • N2 or N3,
  • Levels IV or V nodes,
  • perineural invasion,
  • vascular embolism.
195
Q
  1. Radial forearm sensory innervation?
A

Lateral antebrachial cutaneous nerve

196
Q
  1. Fibula flap blood supply?
A

Peroneal artery

197
Q
  1. DCIA (deep circumflex iliac artery) blood supply?
A

Iliac crest blood supply = Deep circumflex iliac artery (DCIA)

Superior gluteal artery is the most common source of bleeding.

198
Q
  1. When is free flap indicated?
A

s/p radiation for soft tissue

199
Q
  1. Oral cavity SCC location with highest cervical mets rate
A

Tongue (or FOM)

200
Q
  1. BSSO brisk bleeding likely from which artery?
A

Inferior alveolar

201
Q
  1. Long QT syndrome leads to what complication?
A

Torsades de Pointes
Long QT syndrome (LQTS) is a condition which affects repolarization of the heart after a heartbeat. This results in an increased risk of an irregular heartbeat which can result in palpitations, fainting, drowning, or sudden death.
These episodes can be triggered by exercise or stress. Leads to Torsades de Pointes

202
Q
  1. Restylane degradation
A

ans WATER REPLACEMENT
- Short acting hyaluronic acid - dermal filler
- Hyaluronidases are enzymes (endoglycosidases / hyaluronoglucosidases) that hydrolyzes (catalyzes the breakdown of) hyaluronic acid, by cleaving the (1->4)-linkages between N-acetylglucosamine and glucuronate.
- The degradation products of hyaluronan (hyaluronic acid), the oligosaccharides and very low-molecular- weight hyaluronan, exhibit pro-angiogenic properties. Recent studies showed hyaluronan fragments, not the native high-molecular weight molecule, can induce inflammatory responses in macrophages and dendritic cells in tissue injury and in skin transplant.
The answer is water replacement, that is mechanism of restylene

203
Q
  1. Which has worst predictability for soft tissue graft around implant
A

STSG, alloderm, subepithelial CT graft? =

It is alloderm

THIS HAS NOT BEEN CONFIRMED

204
Q
  1. Central incisor with gingival recession, treatment of choice?
A

Connective tissue graft. If recession is above MGJ then success of full to majority of coverage is very high with excellent color match. Success or amount of coverage decreases if recession goes below MGJ (?).

205
Q
  1. Facial widening due to which fracture OF THE MANDIBLE
A

SYMPHYSIS

206
Q
  1. Unilateral condylar fracture, what happens to ipsilateral and contralateral occlusion, and chin deviation? =
A
  1. Ipsilateral occlusal prematurity
  2. Ipsilateral laterognathia (deviation)
  3. Ipsilateral deviation on opening
  4. Contralateral open bite
  5. Inability to achieve MICP
207
Q
  1. SUPERIOR Lateral pterygoid insertions?
A

Medial Disk and capsule
Pterygoid fovea (medial pole of condyle), articular disk (medial aspect). These are the superior head…
Larger inferior head originates from the lateral surface of the lateral pterygoid plate - pass superiorly and outward to fuse with the fibers of the superior head at the neck of the mandibular condyle - insert into the pterygoid fovea.
Superior head originates from the infratemporal surface of the greater sphenoid wing - pass inferiorly, posteriorly and outward - insert in the superior aspect of the pterygoid fovea, the articular capsule and the articular disk at its medial aspect, and the medial pole of the condyle.

208
Q
  1. Progressive edema of upper eyelid?
A

Blepharochalasis

209
Q

c. Blepharochalasis

A

inflammatory component to redundant skin of the lids; relaxation of orbital skin with herniation of upper lid orbital fat (less common than dermatochalasis); often related to angioedema and episodic swelling and edema of the periorbital region

210
Q

b. Pseudodermatochalasis

A

lateral hooding of upper lids due to sagging of forehead skin

211
Q

d. Blepharoptosis

A
  • low-lying upper eyelid margin

Drooping of the eyelid

212
Q

C7-C8 nerve damage symptoms

A

-Paralysis in the legs, torso, and/or hands.
-Inability to control nerves that impact wrist extension.
-Inability to control bladder and bowel function.
-Ability to speak, but breathing may be taxed.

213
Q

If nerve roots of C7-C8 are impacted.

A

C7-T1 (C8 nerve root):
-Pain, tingling, and/or numbness may be felt in the outer forearm and pinky side of the hand.
-Weakness may also be experienced in finger flexors (handgrip) and other muscles.

214
Q
  1. Diagnostic test for parotid tumor with induration and facial nerve involvement

: incision biopsy or FNA? =

A

= FNA before incisional if any concern for malignancy.
FNA is most useful in distinguishing between primary salivary tumors and non-neoplastic inflammatory or infectious processes, lymphoma, and metastases from other nonsalivary primary sites. FNA is performed with a 21-gauge needle and has a 79% accuracy in discriminating between benign and malignant histology. Judicious use of immunohistochemical stains assists in differentiating between benign and malignant tumors; however, there is still a high false-negative rate such that cancer cannot ever be adequately ruled out with needle biopsy. Even so, an incisional biopsy should never be performed on an indeterminate FNA because this may place the facial nerve at risk and increase the risk of recurrence. An ultrasound-guided core needle biopsy is an alternative safe option for tissue sampling and enhanced diagnostic accuracy.

215
Q

Most common fungal infection of the sinus

A

aspergillus.

Clinical manifestations vary depending on the host immune status. Normally it appears as an allergy (allergic fungal sinusitis) or the bronchopulmonary tract. Mass can be established in sinus as a mass of fungal hyphae called aspergilloma. It can calcify becoming an antrolith.
Oral aspergillosis can occur after extraction, as local erythema and pain. Disseminated aspergillosis occurs principally in immunocompromised patients.
Allergic fungal sinusitis treated with debridement and corticosteroids. For invasive aspergillosis, debridement and voriconazole.
Aspergillus forms fruiting bodies and septae branching at acute angles.

216
Q
  1. On panorex how do you tell there is one fracture or two isolated fractures? =
A

The fracture lines converge at inferior border.

217
Q
  1. What is true of VPI in cleft patient requiring maxillary advancement?
A

= No difference in VPI rates for DO vs orthognathic surgery

218
Q
  1. Cleft lip/plate demographics?
A

= CLP overall 1:700 (1:660 in North America)
Blacks 1:2000
Whites 1:1000
Asians 1:500
Native American Indians 1:250-1:500
Males 2:1, Left > Right > Bilateral (6:3:1)
= Isolated cleft palate incidence 1:2000 overall Females 2:1, 50% syndromic

219
Q
  1. Treacher Collins is disruption of which branchial arches
A

first and second branchial arches (same w/ HFM) (1 = maxilla and mandible, 2 = the middle ear.)

220
Q
  1. Where is best skin graft harvest site for nose defect?
A

Lateral neck???
Preauricular vs post auricular region

NOT CONFIRMED

221
Q
  1. Mandible is what type of lever?
A

Class III lever

222
Q
  1. What is a sign of condylar parafunction: vascularity of disc? Fibrocartilage on disc? Thickening of eminence?
A

a. Disc is avascular dense fibrous connective tissue. So vasc is wrong. Unclear. Other tests say collagen, this is correct.

223
Q
  1. Where is the facial nerve located (fascial plane)?
A

Above zygoma: Between TP fascia and Temporal fascia (deep temporalis) Below zygoma: Between SMAS and PM fascia
Galea aponeurotica = TP fascia = SMAS = Platysma Pericranium = Temporalis fascia = PM fascia = SLDCF

224
Q
  1. Rhytidectomy immediately post up with buccal branch weakness, cause?
A

Edema
= Edema, yes or traction

Transient nerve dysfunction in the immediate postoperative period is normal, as a result of edema, prolonged effect of local anesthetics, or traction on the nerve. Spontaneous recovery is noted either early in the postoperative period in the case of edema or prolonged effect of local anesthesia, or later by 3 to 4 months in cases of substantial nerve traction or dissection. Buccal branch is the most commonly injured, but because of the great arborization of this branch, injuries are often less clinically significant compared w/ injury to other facial n branches.

225
Q
  1. Scapular flap blood supply?
A

Circumflex scapular artery

226
Q
  1. Why do gases work faster on peds
A

Alveolar ventilation

227
Q
  1. Problems with Distraction Osteogenesis of anterior defect?
A

issues with vector control

228
Q
  1. Least stable orthognathic movement
A

of what they have listed the answer is maxilla wider
3 least stable (from most stable to least):
Mandible back > Maxilla down > Maxilla wider

229
Q

Septal deviation 1 week after orthognathic surgery?

A

Immediate correction (if not septoplasty in future) If septal deviation is due to lack of appropriate prevention during surgery, or if postoperative manipulation fails to result in correction, immediate reoperation with caudal septal resection, is warranted. If these approaches are not acceptable to either the patient or the surgeon and the patient does not have any significant airway difficulties or cosmetic concerns, the septal deviation may be reevaluated at a later date with consideration for a standard septoplasty procedure. Petersons pg 1440

230
Q
  1. Maxillary osteosarcoma with positive margin superiorly
A

interarterial chemo

= Chemo -> resection -> chemo
From Cancer center, interarterial chemo is the answer, even though that’s kind of weird.

231
Q
  1. NBCC / Gorlin syndrome:

23 symptoms

A

BCC, neurologic syndromes; picture of a basal cell carcinoma on philtrum
= 50% or greater frequency:
-Calcified falx cerebri /
-OKCs /
-Multiple BCCs /
-Epidermoid cysts /
-Spina bifida /
-Palmar + plantar pits /
-Enlarged head circumference /
-Rib abnormalities (bifid) /
-Mild ocular hypertelorism.
-15%-49%: calcified ovarian fibromas,
-short fourth metacarpals,
-kyphoscoliosis,
-pectus excavatum,
-strabismus
-<15%: medulloblastoma,
-meningioma,
-lymphomesenteric cysts,
-cardiac fibroma,
-fetal rhabdomyoma,
-marfanoid build,
-cleft lip/palate,
-hypogonadism,
-mental retardation / neurologic

232
Q

Which syndrome is associated with multiple OKCs

A

Nevoid basal cell carcinoma (Gorlin-Goltz syndrome)

233
Q
  1. What is contraindication to use of Champy plate in mandibular angle fracture?
A

Comminution inferior border

234
Q
  1. What happens if medial cut of BSSO too high?
A

condyle in distal segment

235
Q
  1. How to distinguish Guillain Barre from periodic familial paralysis?
A

Potassium Periodic paralysis mimics Guillain-Barre and can be either hyper or hypokalemic in origin.
GB = normokalemia; PFP = hypokalemia/hyper. Guillain-Barre will present as hyponatremic.

Potassium is the answer

236
Q
  1. What is junctional rhythm?
A

Cardiac rhythms arising from atrioventricular (AV) junction occur as an automatic tachycardia or escape mechanism during periods of significant bradycardia w/ rates slower than the intrinsic junctional pacemaker.
- The AV node has intrinsic automaticity that allows it to initiate and depolarize the myocardium during periods of significant SBrady or complete heart block. This escape mechanism, with a rate of 40-60 beats per minute, produces a narrow QRS complex because the ventricle is depolarized using the normal conduction pathway.

  • Junctional rhythm can be diagnosed on an ECG: it usually presents without a P wave or with an inverted P wave. Retrograde P waves refers to the depolarization from the AV node back towards the SA node.
    x
237
Q
  1. Most common site of clot leading to PE?
A

iliofemoral? Was the closest thing they had to deep proximal DVT
= Proximal DVT (poplitial, femoral, iliac). (90% of emboli from proximal leg deep vein or pelvic vein thromboses). DVTs are located in the posterior tibial and peroneal veins (muscular calf veins) while anterior tibial and muscular vein DVTs are uncommon.

238
Q
  1. Cardiac complication of OSA? =

(6 pts)

A

endothelial dysfunction in OSA leading to increased cardiovascular risk

-HTN,
-stroke,
-Afib,
-CHF,
-CAD,
-sudden cardiac death.
Patients with severe OSA exhibit a higher prevalence of coronary artery disease, heart failure and stroke. The mechanisms behind increased cardiovascular risk in OSA remain elusive. Several theories have been postulated, including sympathetic activation, oxidative stress and inflammation.

Endothelial injury results in alteration of endothelial hormones that are responsible for maintaining vascular tone and preventing abnormal cell proliferation, increased coagulability and altered leukocyte trafficking; and exposes subendothelial structures to diverse growth factors in the blood.4 The resultant vasoconstriction, vascular smooth muscle proliferation, and hypercoagulability may lead to adverse cardiovascular consequences associated with OSA, such as hypertension, coronary artery disease, and cerebrovascular disease.

Endothelial dysfunction may be another link between OSA and cardiovascular disease. Dysfunctional endothelium is characterized by an imbalance in production of vasoactive hormones, increased adherence of inflammatory mediators to endothelial cells and hypercoagulability, and is a known risk factor for cardiovascular events. Studies have directly measured vascular endothelial function in patients with OSA and found a muted response compared to control

239
Q
  1. What is second degree type II heart block? =
A

Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening. There is usually a fixed number of non-conducted P waves for every successfully conducted QRS complex, and this ratio is often specified in describing Mobitz II blocks, 2:1 or 3:1 P:QRS ratio. Definitive treatment = pacemaker.

240
Q
  1. Thalassemia can cause
A

VME

241
Q
  1. Treatment for 5 year old boy with condylar agenesis
A

Answer is costo condral graft
watch and wait, functional appliance, surgery?
- If the condition is syndromic or progressive, I believe you need to do a costochondral graft before puberty to avoid massive asymmetry.
- If it is simple agenesis with otherwise normal anatomy and the patient is cooperative, positive outcomes can be attained with ortho appliances alone.

242
Q
  1. Coronectomy facts: same morbidity? Root migration? =
A

Root migration: Most root migration was found to occur within 6 months (91.1%) and 12 months (61.4%) postoperative. From 24 months onwards, less than 5% migrated further. Age was found to be a factor affecting root migration: migration decreased with increasing age (by 0.203mm less per year increase in age). Other factors investigated were found to be unrelated. Root migration pattern after third molar coronectomy: a long-term analysis. Int J Oral Maxillofac Surg. 2018 Jun;47(6):802-808

Morbidity: The prevalence of IAN injury was 0.16% (1/612) and was temporary. Long-term postoperative infection occurred in 1 case at 6 months following surgery and another at 12 months. No infection was found after 12 months. The incidence rates of pain at 6 months, 12 months, 24 months after surgery were 0.50% (3/596), 0.38% (2/529), 0.49% (2/411), respectively. Root exposure was noted in 2.3% of cases (14/612). Reoperation to remove the exposed root did not cause any IAN deficit

243
Q
  1. Obese patient changes in FRC, FEV, FVC? =
A

Obesity is more associated with restrictive lung the obstructive

Decreased FRC, FEV1, FVC (FEV1/FVC ratio normal to increased; restrictive lung disease)
Chest wall and lung compliance is decreased from the accumulation of fat on the thorax and abdomen. Decreased pulmonary compliance leads to decreased FRC (primarily a result of lowered ERV), VC, and TLC.

FRC-Functional residual capacity (FRC), is the volume remaining in the lungs after a normal, passive exhalation (about 3 L)
FEV1-FEV1 is the amount of air you can force from your lungs in one second.
FVC-orced vital capacity (FVC) is the total amount of air exhaled during the FEV test.

244
Q

When compming a morbidly obese patjent to a non-obese patient, which of the following statements is conect?

A. Oxygen consumption is higher in the non-obese patient.

B. Functional residual capacity is the same.

C. Time to desaturation with a period of apnea is the same.

D. Positioning may diminish pulmonary reserve more in the obese patient.

A

Answer: D Rationale:
Patients who are morbidly obese have changes in pulmonary, cardiovascular, gastrointestinal, and metabolic systems. Patients who are morbidly obese have increased minute ventilation at rest to meet the metabolic needs of the increased tissue mass. Changes in lung volumes at rest include reduced FRC, vital capacity, and total lung capacity. Closing volume is unchanged and reduced FRC can result in lung volumes below closing capacity in normal tidal ventilation. Anesthesia compounds these problems with greater reductions in FRC in obese patients compared to nonobese patients of the same age. As a result, obese patient’s ability to tolerate periods of apnea is reduced. Patient positioning aggravates these changes in lung volumes and conttibutes to poor respiratmy reserve in obese patients. Reverse Trendelenberg is the most optimal position for lung volumes whereas supine positjon and Trendelenberg are worst in terms of safe apnea periods and recovery time.

245
Q

Which statement is accurate regarding the morbidly obese patient?

A. Functional residual capacity is maintained.
B. Obesity imposes an obstrnctive ventilation defect.
C. PaO2 is decreased reflecting ventilation - perfusion mismatching.
D. PaCO2 increases slightly secondary to a slight decrease in the ventilatory response to CO2_

A

Answer: C

Rationale:
Morbid obesity is defined as a body weight in excess of 100 lbs over ideal weight or a body mass index of 40 or greater. There are a variety of adverse changes associated with obesity. Pulmonmy function changes in obese patients suggest restrictive pulmonary disease characteristics. PaO2 is decreased by obesity as a result of ventilation/perfusion mismatches. Despite this, PaCO2 and the ventilatory response to PaCO2 remains normal. Functional residual capacity is decreased and is accentuated by supine positioning and milder anesthesia.

246
Q

A healthy 22 year-old female who is 5 foot 2 inches, 170 pounds presents for extraction of 1 tooth. Oxygen at 4 liters/minute is administered via nasal cannula. Five minutes after oxygen administration is initiated the patient is induced with propofol 140 mgs. The patient becomes apneic. Pulse oximeter reads 100%. The surgeon proceeds with extracting the tooth and does not take immediate intervention to provide airway support and positive pressure ventilation.
Which of the following either justifies or counters the surgeon’s actions?

A. Preoxygenationwith the 36% oxygen mixture for 5 minutes will maintain the oxygen saturation at or above 90% for at least 3 minutes in this individual

B. The surgeon should initiate positive pressure ventilation as obese patients desaturate approximately twice as rapidly as individuals with lean body mass.

C. Preoxygenation with an FiOiof 0.36 will produce a PAo, of 160 mm Hg which does not provide ample reserve for the surgeon to complete a 30 second procedure

D. The administration of propofol will not result in prolonged apnea and continuous insufflation of oxygen will sustain an oxyhemoglobin saturation > 90%.

A

Answer: B Rationale:
Preoxygenation is the process of administering oxygen to a patient prior to inducing anesthesia. The intent is to replace the volume of nitrogen in the lungs with oxygen (denitrogenation). PA02is calculated using the formula PA02 = F;O2 (P8-PH2o)­ P3CO2/RQ where P8 = 760, and PaCOi/RQ = 40/0.8. Preoxygenation provides a reservoir of oxygen occupying the functional residual capacity that can diffuse into the alveolar capillaries and provide oxygen during periods of hypoventilation and apnea. Preoxygenation with 100% oxygen for 5 minutes can provide up to 10 minutes of oxygen reserve to a healthy individual during periods of apnea and normal oxygen utilization. In one study comparing healthy individuals of ideal weight to obese individuals who were preoxygenated with 100% oxygen, the obese individuals desaturated to an oxygen
saturation < 90% approximately twice as fast as the nonobese individuals (2.7 minutes
compared to 6 minutes). In another study a nonobese patient breathing room air will desaturate to an oxygen saturation < 90% in about 2 minutes.

Achievement of a general anesthetic depth solely with propofol will be more predictable in its recovery. However, the apneic patient, especially the obese patient, cannot rely on recovery from the propofol bolus and resumption of ventilation to maintain oxygenation. Apneic oxygenation is a technique that is dependent on pharyngeal insufflation of oxygen. This technique is dependent on more oxygen diffusing out of the alveoli into the capillaries than carbon dioxide diffusing into from the capillaries into the alveoli. This decrease in intrathoracic pressure relative to atmospheric pressure facilitates oxygen delivery. Carbon dioxide is not removed from the alveoli limiting the duration of this oxygenation technique. Apneic oxygenation is dependent on a patent airway. It is most likely that a bolus of propofol that produces apnea also compromises airway patency.

247
Q

Which of the foUowing best characterize restrictive lung disease?

A. Decrease in total lung capacity

B. Decrease in iFEVl/FVC rntio

C. increase in vital capacity

D. Increase in airway resistance

A

Answer: A

Rationale:
Restrictive disorders are best evaluated by measuring 11mg volumes. The severity of the restrictive defect is based on the TLC (total lung capacity). In restrictive lung disorders, the FEVl may be decreased, but the FEVl/FVC ratio will be preserved. The TLC, FRC (functional residual capacity) and RV (residual volume) will all be decreased, Airway resistance is not affected in a restrictive lung disease.

Restrictive disorders can occur in three circumstances: lung disorders, disorders of the chest wall and neumnmscular disease. Lung disorders with interstitial infiltration typically show restriction caused by increased elastic recoil such as observed in idiopathic pulmonary fibrosis and sarcoidosis. Lung edema as a result of congestive heart failure can also cause a restrictive pattern. Chest wall abnormalities may exhibit themselves with a restrictive pattern by restricting 1mg expansion as observed clinically in kyphoscoliosis, obesity, and ankylosing spondylitis Included in the chest wall abnormalities are the pleural diseases (pleural effusion, pneumothorax,), space occupying lesions (tumors), and conditions causing increased abdominal girth such as pregnancy, a.sci.ks, and large intraabdominal tumors. Some neuromuscular disorders ,cause restriction by preventing normal excursion of the hmg during breathing as observe,d in patients with myasthenia gravis, amyotrnphic lateral sclerosis, diaphragmatic paralysis and the Guillain-Barre syndrome. Patients may also restrict lung excursion during inspiration as a result of pain or somnolence (drug overdo e). Lung resection during lobectomy will also c.ause a restrictive defect.

Decrease in the FEVl/FVC ratio is the hallmark of obstructive lung disease. Airway resistance is increased in obstructive lung disease (asthma).

248
Q

A 36-year-old obese female is in your office requesting a general anesthetic for extraction of a carious tooth. Your primary concern in regards to her obesity and pulmonary function is:

A a decreased FEV1
B. a decreased functional residual capacity.
C. a decreased minute ventilation.
D. a decreased residual volume.

A

Answer: B

Rationale:
Morbid obesity is charncterized by reductions in functional residual capacity (FRC= volume remaining in the lungs after a normal quiet expiration), expiratory reserve volume (ERV=volume of air that can forcefully expired after a normal resting expiration) and total lung capacity (TLC). These changes have been attTibuted to mass loading and splinting of the diaphragm. Anesthesia compounds these problems and impairs the ability of the obese to tolerate periods of apnea. Residual volume consists of the gases remaining in the lung after a forced expiration and is less variable than other parnmeters. FEVl is the forced expiratory volume in 1 second and is most often used as a determinant of inflammation and small airway obstruction in obstructive lung diseases such as asthma.

249
Q
  1. What happens if TAD implant hits dentin?
A

External resorption was closest thing to reparative cementum

  • If root damage is included inside of cementum and dentin, a repairing mechanism by periodontal tissues works well, and no serious problem will occur clinically. Ahmed et al. evaluated the reparative potential of cementum histologically after intentional root contact with a miniscrew. The roots of the premolars were intentionally injured with a miniscrews and extracted at 4, 8, or 12 weeks after the injury. Despite varying depths of the injuries, including involvement of dentin, reparative cementum formation was observed in all sections. Healing cementum was almost exclusively of the cellular type; 70% of all the teeth exhibited good repair by the end of week
    12. Conclusively, this study established that healing of cementum takes place after an injury with a miniscrew, and it is a time-dependent phenomenon. On the other hand, root damage through the dental pulp is irreversible, and root canal filling after pulpectomy or tooth extraction should be necessary.
250
Q

What is surface respiration, replacement resorption, and inflammatory resorption

A
  • Surface resorption: a luxated or avulsed tooth root displays superficial resorption lacunae, which are repaired with newly formed cementum. This development is a response to localized PDL or cementum injury.
  • Replacement resorption: ankylosis, there is a merging of bone and the root substance. Root substance is replaced by bone.
  • Inflammatory resorption: well circumscribed areas of cementum and dentin resorption. The localized periodontal tissue is inflamed. The onset of inflammation is a result of the infected and necrotic pulp tissue within the root canal.
251
Q
  1. How long to wait after URI prior to surgery?
A

answer is 2-6 weeks
- Bronchial hypersensitivity may last 4-6 weeks after URI; recommended to delay treatment for at least 6 weeks.
- If urgent or ER surgery needed, LMA may reduce complications.
- Irritable airway, increased risk of laryngospasm, bronchospams, postintubation croup (peds), pneumonia, and episodes of desaturation. Signs of URI = fever, fatigue, loss of appetite, productive cough, thick nasal discharge.
- Delaying surgery does not reduce the incidence of adverse respiratory events if the patient undergoes anesthesia within 4 weeks of the URI. Airway hyperrreactivity may require 6 weeks or more to abate.- stoeltings pg 182.

252
Q

1) A pt with myasthenia gravis is undergoing I&D under GA and has acute onset of hypotension (70/40). What would you do first?

A

b. Vasopressors etc.

253
Q

Patient had I and D under local. Went into myasthenic crisis. Now intubated on vent. What do you do now?

a. high dose steroid
b. plasmapheresis
c. IVIG
d. stop anticholinesterase

A

-plasmapheresis

Plasmapheresis involves removing blood through a needle or catheter and circulating it through a machine where the blood is separated into red cells, white cells, platelets and plasma. The plasma, which is the fluid content of the blood, is discarded and replaced with a substitution fluid (mainly albumin solution)

254
Q

1) What medication should you avoid in the Myasthenia Gravis patient?

A

Beta blockers, CCB, muscle relaxants

255
Q
  1. Preop management of Myasthenia Gravis patient.
A
  • Give preop NSAID
  • plasmaphoresis
  • stress dose prednisone
  • The answer is probably stress dose steroids. There can be adrenal suppression and other axis suppression issues, NSAIDs can help but that’s not really a good answer here and plasma exchange is an emergent therapy not a routine pre-op.
256
Q
  1. Myasthenia Gravis patient sensitive to what?
A
  • Atracurium

Any Non-depolarizing NMB is probably the answer they are shooting for, these patients are extremely sensitive.

Examples of non-depolarizing meds include
(e.g., rocuronium, vecuronium, pancuronium) or benzylisoquinolinium (e.g., mivacurium, atracurium, cisatracurium).

257
Q

Myasthesthenia gravis questions

( 5 pts)

A
  1. Preop give steroids
  2. Intraop htn give vasopressors (if BP goes down)
  3. Post op plasmapheresis
  4. Absolutely avoid beta blockers (also CCBs)
  5. They are sensitive to ROC but not as dangerous as beta blockers
258
Q

1) Using peridex as a pre-op mouth rinse decreases chances of pneumonia by what percentage?
a. 5,35,60,80 (50-60%)

A

60

259
Q

2) A patient is diabetic with proteinuria and CrCl of 35, what is going on?

a. Cystitis
b. Glomerulosclerosis
c. Stage 5 Renal disease
d. Pyelonephritis

A

Glomerulosclerosis??

Feeling pretty sure based on what I’ve read

260
Q

3) Bump on gum present for 4mos, occasional bleeding when touching lesion, that is “clinically firm”
a. POF
b. Peripheral Central Giant Cell
c. Pyogenic granuloma
LOOKED LIKE GIANT CELLS ON HISTO

A

b. Peripheral Central Giant Cell

261
Q

4) Ferric 3+ is in what form
a. Oxidized Fe 3+
b. Reduced Fe 3+
c. Oxidized Fe 2+
d. Reduced Fe 2+

A

Oxidized Fe 3+ (CORRECT ANSWER)

262
Q

5) What week does palatal arches fuse

A

a. 6-10 weeks

263
Q

6) Embryonic origination of junctional epithelium

A

a. reduced enamel epithelium (REE)

264
Q

7) immediate provisionalization preserves

A

a. Marginal soft tissue and crestal bone

265
Q

8) Early vs late implant failure similarities

A

a. Parafunction

266
Q

9) Implant placed too facial

A

a. Place more palatally

267
Q

10) EtCO2 capnography with with decrease RR and increasing etco2

A

a. Administer naloxone

268
Q

12) Protein C is a

A

a. major physiologic anticoagulant

269
Q

13) coronectomy, important step

A

a. remove all enamel

270
Q

14) most common immediate complication of coronectomy

a. BOP???
b. Dry socket
c. Late infection
d. Neurosensory disturbance

A

a. BOP???

271
Q

15) Severe odontogenic infection and in sepsis, which GA will you use
a. Isoflurane
b. Desflurane
c. Sevoflurane
d. Propofol

A

c. Sevoflurane

When neutrophils were exposed to sevoflurane in a dish, they also showed reduced apoptosis. Molecular studies showed that sevoflurane blocked the binding of two proteins in the Fas apoptosis pathway, known as Fas D and FADD.

Less bacteria than isoflurance in sepsis mice

272
Q

16) Substance P causes

A

vasodilation

Substance P’s most well-known function is as a neurotransmitter and a modulator of pain perception by altering cellular signaling pathways. Additionally, substance P plays a role in gastrointestinal functioning, memory processing, angiogenesis, vasodilation, and cell growth and proliferation

273
Q

17) What does not prolong QT interval
a. Ketamine
b. Versed
c. Succinylcholine
d. Glycopyrrolate

A

Versed

Avoid ketamine, succinylcholine and glycopyrrolate

274
Q

18) Sedation on ex-premature

A

a. Bronchopulmonary dysfunction??

275
Q

19) 10cm x 7cm defect s/p excision of cancer to retromolar trigone, how to recon?

a. Submental island flap
b. Pec
c. Lat Dorsi
d. Cervicofacial

A

submental island flap

Likely pec flap according to John

276
Q

20) Anticoagulation for flaps in kid

A

a. Dextran

277
Q

22) TCA

A

a. Nociceptive pathway’

Tricyclic antidepressants may relieve neuropathic pain by their unique ability to inhibit presynaptic reuptake of the biogenic amines serotonin and noradrenaline, but other mechanisms such as N-methyl-D-aspartate receptor and ion channel blockade probably also play a role in their pain-relieving effect.

TCAs include
Amitriptyline.
Amoxapine.
Desipramine (Norpramin)
Doxepin.
Imipramine (Tofranil)
Nortriptyline (Pamelor)
Protriptyline.
Trimipramine.

278
Q

23) Which level for triceps dysfunction

A

a. C7-C8

279
Q

24) Mechanism of propofol induced bradycardia

A

a. Inhibition of baroreceptor
i. (The normal arterial baroreflex response to hypotension appears blunted by propofol; furthermore, significant preload reduction can result in vagal-mediated reflex bradycardia.)

b. Decrease in arterial pressure

280
Q

25) Apfel score (risk of PONV)

A

Purpose: The Apfel simplified risk score, developed in 1999, is the most widely used tool for risk stratification of postoperative nausea and vomiting (PONV). It includes four risk factors: female sex, non-smoking status, history of PONV or motion sickness, and use of postoperative opioids

Each point increase risk of PONV.

281
Q

26) Bone graft in sinus, which resorbs the quickest

A

a. Xenograft
b. Allograft (resorbs quickest)
c. Auto particulate graft
d. Alloplastic

Allograft-a tissue graft from a donor of the same species as the recipient but not genetically identical.

282
Q
A

Ameloblastoma

283
Q
A

Warthin’s Tumor

284
Q

Warthin’s tumor histology

A
285
Q
A

Acute myeloid leukemia

286
Q

32) Murmur with wide split S2, anesthetic complication

A

he second heart sounds are best heard in the second and third left intercostal spaces. The second heart sound (S2) represents closure of the aortic (A2) and pulmonary (P2) valves at the end of systole, in that order. An accurate assessment of the quality of this heart sound is critical in a thorough cardiac examination. Under normal circumstances, systemic vascular resistance (SVR) is higher than pulmonary vascular resistance (PVR), allowing slightly longer systolic ejection time into the pulmonary bed. As a result, the aortic valve closes before the pulmonary valve (A2P2). This splitting of S2 also varies with the respiratory cycle. During inspiration, increased central venous return to the right heart takes longer to cross the right ventricular outflow tract. Closure of the pulmonary valve is delayed compared to the ejection time in expiration; thus, the aortic and pulmonic components of S2 are more readily separated from each other in inspiration. This variability in the timing of A2 and P2 with the respiratory cycle is termed physiologic splitting. If this variability is not appreciated beyond infancy or at slower heart rates, an abnormality of the cardiopulmonary system must be suspected.

287
Q

33) Atrophic mandible, healing compromised

A

a. Decreased IA artery profusion

Yep, remember as mandibles age and atrophy, more blood supply comes from periosteum (centripetally).

288
Q

34) Patient taking Denosumab s/p cancer, tooth extracted, 8 weeks later develops ONJ

A

a. MRONJ

289
Q

35) Lateral ceph s/p lefort

A

a. Nasotracheal intubation

290
Q

36) Sintering (processing) xenograft

A

a. Slows resorption-CONFIRTMED

hus, heat treatment with different sintering temperatures has been outlined as a crucial manufacturing step that affects the material characteristics and the subsequent reactions to these materials.18,19 High processing temperatures are thought to be necessary for the complete deactivation of pathogens to prevent cross-infections.19 Indeed, Goller et al19 postulated that densification and mechanical properties steadily improve with increasing sintering temperature and that sintering at the higher temperatures of 1200°C and 1300°C yields significantly denser and stronger materials.

291
Q

37) GCS 12

A

What kind of head trauma-Moderate

292
Q

38) After fracture, what increases postop infection rate

a. Removing 3rd molar at time of fixation
b. Delaying 5 days
c. Non-rigid fixation

A

Non-rigid fixation

293
Q

39) Blunt/penetrating trauma to mandible, which blood vessel most likely at

a. Internal carotid
b. Common carotid
c. External jugular

A

a. Internal carotid

294
Q

40) EtCO2 capnography

A

a. Hyperventilation

295
Q

41) Max Dose dantrolene

A

a. 10mg/kg, confirmed

296
Q

42) What defines nasal fat pad

A

b. Inferior oblique (I think)

The inferior oblique is reliably located in the cleft between the nasal and central fat pads. Using cotton-tipped applicators, the nasal and central fat pads can be easily separated to allow the inferior oblique to come into view. Once identified, one can safely proceed with excision of the fat pads

297
Q

43) Immediate implant failure

A

a. Inadequate bone grafting between implant and alveolus

298
Q

44) Zygomatic implant placed with good stability in optimal location, 2 months after loading oral antral communication forms, what to do
a. Remove
b. Buccal fat graft (I guessed)
c. Take it out and place it out of the sinus

A

b. Buccal fat graft (I guessed)

299
Q

Drugs to avoid in WPW

A

AABCD
A-Adenosine
A-Amiodarone
B-Beta Blockers
C-Calcium channel blockers
D-Digoxin

300
Q

Tardive dyskineasia

A

a condition where your face, body or both make sudden, irregular movements which you cannot control.

Tardive dyskinesia (TD) is a drug-induced involuntary movement disorder, generally of the lower face including the jaw, lips and tongue.1,2 It can also affect the trunk and extremities. The term tardive means “delayed”, and dyskinesia means “abnormal movement”.1 People with Parkinson’s disease (PD) are familiar with the feeling of uncontrolled movements. TD can affect those with or without PD or other movement disorders. The symptoms of tardive dyskinesia are brought on by the medications that are used to treat Parkinson’s and other conditions.

he symptoms develop after taking neuroleptics, dopamine receptor blocking drugs (DRBD),

301
Q
A

Histology of a giant cell tumor