PhamBam Flashcards
Primary HyperPTH diagnostic test?
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
Primary hyperPTH phosphate?
= low phosphate
What is the most common cause of secondary hyperparathyroidism?
Chronic Kidney disease?
In primary hyperparathyroidism, what is the calcium, phosphate & all phos labs look like
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.
In secondary hyperparathyroidism, what is the calcium, phosphate & all phos labs look like
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.
In paraneoplastic hyperparathyroidism, what is the calcium, phosphate & all phos labs look like
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.
Describe calcium phosphate, and all phos levels in…
Paget’s Disease
Cherubsim
Fibrous Dysplasia
Ossifying firm
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.
- Obstructive and restrictive lung disease similarity?
SAME TIDAL VOLUME
= reduced FEV1, unchanged TV, SOB with exertion and
What is the difference between Obstructive and Restrictive/obesity lung volumes
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.
Difference between obstruction and restrictive lung diseases
Looks like total lung capacity in obstructive lung disease is higher.
- What is Protein C?
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
- First degree block treatment?
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
- Reversible asthma FEV? = answer 12% and 200mL
= Reversibility is present if there is at least a 12% and 200mL increase in the FEV1 after bronchodilator given.
Multiple sclerosis = answer was 3 key words
Auto immune central demyelination
- Serotonin syndrome treatment?
Cyproheptadine H1 antagonist (antihistamine)
At high concentrations, has antiserotonergic (5HT2 – excellent for tx of SS), anticholinergic, antidopaminergic effects.
Symptoms of Serotonin Syndrome:
tremors, myoclonus, hyperreflexia, mydriasis, GI symptoms (N/V/D).
Five principles are central to the management of serotonin syndrome:
- 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
Which drug may induce Serotonin syndrome when combined with a selective serotonin reuptake inhibitor.
Alafentanil
Fentanyl
Meperiidine
Morphine
Meperidine
Serotonin syndrome is characterized by confusion agitation tachycardia, fever, hyperreflexia, mydriasis, myoclonus. Normeperidine is an active metabolite of meperidine
- Transfusion related complication?
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.
- Phenytoin and Tylenol toxicity
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.
- EKG of WPW (Wolf-Parkinson-White
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).
Which medication should you not use in WPW
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.
Wolff-Parkinson-White
What is it, what symptoms, and what treatment.
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.
Wolfe Parkinson White Syndrome
The medical treatment for WPW syndrome
procainamide (sodium channel blocker, Class I-A antiarrhythmic drug).
- Methemoglobinemia question, what is it, answer OXIDIZED Fe3+ (causes L shift of HgB affinity)
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.
When methemoglobin concentration is elevated in red blood cells what occurs
associated oxygen–hemoglobin dissociation curve shifted to the left, tissue hypoxia may occur.
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
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.
Answer is methylene blue administration of 1 mg/kg IV
- Why do anesthetic gases work faster for peds pts?
Higher alveolar ventilation (and lower FRC).
- Why do gases work faster for peds pts
(8 pts)
- 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
A few reminders about infants when considering pharmacology.
5 points
: 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.
Compared to adults, what do infants hav min terms of alveolar ventilation and FRC?
. 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).
- Ketamine IM dose Peds?
= 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
- Zofran MOA
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).
- Parkinson’s disease, what drugs should you avoid.
DM in the pM
- 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).
Parkinson’s disease
(4 main points)
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.
c. Dopamine depletion in the substantiated nigra of the basal ganglia.
d. Pehnothiazines
These drugs block dopamine receptors and can lead to movement disorder and TMJ dislocation
C. levodopa should be discontinued 24 hrs prior to neuromuscular blocking agent
- Drug that can cause hypertension thereby counteracting the effects of hypertensive meds? =
= Ibuprofen
- Best vagal maneuver for kids?
= 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.
- EtCO2 7mmHG during chest compression, what is the cause?
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.
- How do you treat a wide complex monomorphic tachycardia in a kid who is unstable? =
= Synchronized cardioversion 0.5-1 J/kg, bump it up to 2 J/kg if not effective (PALS)
- Succinylcholine in kids causes what cardiovascular symptoms
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.
- Upslope of EtCO2 curve?
Obstruction, new question said how do you tx, answer maybe suction?
Review how to treat pediatric tachycardia with a pulse and poor perfusion algorithm
- Max dose dantrolene?
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.
Contraindication to LMA?
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
Absolute contraindication to LMA
trismus and complete upper airway obstruction
Relative contraindications to LMA
(8 pts)
- 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
- Hypertrophic Obstructive Cardiomyopathy (HOCM) anesthetic considerations
directed towards minimizing LVOT (Left ventricular outflow tract) obstruction by decreasing myocardial contractility and increasing preload and afterload
Events that decrease outflow tract obstruction
(10 pts)
- 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.
- Erythromycin and versed
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%.
- Dexmedetomidine MOA? =
Also known as Precedex
Central a2 agonist.
(Reversal is atipamezole = synthetic a2 antagonist)
Alpha 2 agonists inhibit norepinephrine, acetylcholine, and insulin
- Treatment of symptomatic bradycardia in peds?
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.
- Damage of lingual nerve causes loss of?
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.
- What does lateral pharyngeal space abscess present as
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.
- Where to I&D for masticator space? =
just inferior and parallel to angle of mandible
Masticator Space = confluence of: submasseteric, pterygomandibular, superficial temporal and deep temporal space.
- Acute hepatotoxicity with Tylenol and what other drug?
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.
- What is substance P? q what does it actually do
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
- Symptoms of superior orbital fissure syndrome?
(5 pts)
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.
What is ophthalmoplegia?
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.
Orbital apex syndrome
(5 symptoms +1)
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.
- Adenosine MOA?
7 pts
= 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.
- What causes V/Q mismatch leading to hypoxemia?
ARDS
- What is point at which elastic recoil of chest and lung are equal?
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.
V/Q mismatch causes (7)
- 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
- What is volume of distribution dependent on?
Answer LIPID SOLUBILITY, Jay went with concentration…
a. Lipid solubility, Non-ionizing drugs, lack of serum protein binding all have high volume of distribution
- What do halogenated anesthetics do to lung?
bronchodilator
Halogenated anesthetics include desflurane, isoflurane, sevoflurane
- What determines slow onset of bupivacaine?
Disassociation constant
a. Onset = pKa, duration of action = protein binding, potency = lipid solubility
- What type of impaction is easiest for coronectomy?
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
- What type of impaction likely to dislodge root in coronectomy?
Distoangular has higher root migration risk
Coronectomy is contraindicated (relative) in horizontal imp d/t increased risk of nerve injury with sectioning (Pogrel).
- Proptosis, periorbital edema after extraction #1
Postseptal/Retroseptal cellulitis (key is proptosis)
- Signs of Cavernous Sinus Thrombosis?
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
- What is true of tooth fracture: apical 1/3 most common?
Ellis III most common? Splint for 2 wks?———
How Ong do root fractures need to be splinted for?
6 weeks
Ellis Classifications
- Goode ratio?
if nasofrontal angle 36-40 then nasal projection should be 0.55-0.60 of nasal dorsum length
- Wallace rule of 9’s
how much surface area burned if head, one upper extremity and anterior torso burned
——- head-9, upper ext 9, torso to include chest and abd 18. (For reference lower ext is 18%)
Type 3 necrotizing fasciitis?
gas gangrene, eg due to clostridium
Types of necrotizing fasciitis
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)
- Cleft palate with chr 22 deletion?
VCF (Velocardiofacial, also DiGeorge).
CATCH-22 (Cardiac anomalies, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia).
- Transcaruncular approach to medial orbital wall, what are anatomic landmarks?
caruncle + semilunar fold.
Incision posterior/lateral to caruncle and anterior/medial to semilunar fold (plica semilunaris).
- What type of flap is buccal fat pad?
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.
- What is a random pattern flap?
No named blood vessel
- GCS scale, question was you were given the actual numbers and had to say mild, MODERATE, severe
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
- Bite wound closure and irrigation?
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.
- Hyphema:
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
- Hyphema: What increase risk of rebleed?
= Stage of hyphema = 50% is increased risk of rebleed.
- Use of ASA or ibuprofen, HTN, increased IOP, African American and hypotony.
- AS above, listed factors for risk of re-bleeding for a hyphema are
- hypotony (IOP of 5 mmHg or less)
- elevated IOP,
- 50% greater hyphema,
- HTN,
- African American
- ASA use
Wat’s the first sign of traumatic optic neuropathy?
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
- How much height needed from ridge for implant supported partial denture?
11mm
- What’s most stable reconstruction for multiple teeth missing
Implant supported FIXED partial?
- Loading force for zygomatic implant and anterior implant
40Ncm
- Tension vs compression zones of mandible?
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.
- Least likely injury to nasolacrimal duct?
Bilateral superior orbital rim fracture? Anterior table comminution? Anterior and posterior table comminution?
- Osteochondroma tumor growth is by what mechanism?
Lichtenstein theory –
osteochondroma develops by the metaplastic changes in the periosteum, as the pluripotent periosteum has the potential to differentiate into osteoblasts and chondroblasts.
- Most common odontogenic tumor?
Odontoma > Amelo
benign most common odontogenic tumor
- CN3 palsy will cause what? Answer DOWN and OUT eyes
(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
- Best method for canalicular repair?
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.
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
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.
Tests for latency of the nasolacrimal duct
. 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.
- Class III malocclusion requiring maxillary advancement and downgrafting—why relapse after one year?
= 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”)
- Crouzon syndrome – what happens to mandible growth?
UNCHANGED
= Mandible growth should remain unaffected
- Indications for uses of oral appliance
= Primary snoring and mild OSA
- Patient with OSA from hypopharynx obstruction, SNA 79 SNB 76 what is best treatment
MMA
- Where do maxillary and mandibular bone come from
Branchial arch 1, mesoderm
Test said ectoderm, but we are sure it is mesoderm
ectoderm
- Palatoplasty most maxillary growth restriction?
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.
- Clover leaf deformity, Kleeblattschadel?
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
- soft tissue change ratio for chin alloplastic implant? =
0.8 to 1.0 hard to soft tissue movement
- lingual frenectomy? How often needed in infants? Changes in latching? Does type of frenectomy affect outcome?
??
ans outcomes do not depend on technique
- High mandibular plane angle and low hyoid causes what
Poor outcome for cosmetic surgery?
- Lower lid retraction? What is distance and time (in sec) that is normal
Peterson says: Snap and distraction 7mm/1sec
Old OMSITE says Snap 1-3secs, and distraction <6mms normal
6mm and 1second
- Tip of nose innervation?
External branch of anterior ethmoid nerve (CNV1).
Can also be innervated by infratrochlear, supratrochlear, and infraorbital.
- Trichophytic brow lift indications in what types of patients? =
= 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.
- Keystone area?
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
- Keystone area? 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
- How does the ULC and LLC joint at the scroll?
Answer interlocking
- Most common complication of alloderm:
? Assuming infection. But can’t