ORAL SURGERY AND PAIN CONTROL

How many milligrams ofepin€phrine are in cach certridge (1.8 cc) of 2oh lidocrine with 1:100,000 epinephrine? 0.018 mg l8 mg 0.036 mg 36 mg

0.018 mg I cc oI2o/o lidocaine with epinephrine 1:100,000 contains the following: . Noaesl - l0 mg of lidocaine: Blockade ofnerve conduction - 0.01 mg ofcpineph ne: lncrease depth and duration ofanesthesia; decrease absorption of local ancsthetic and vasopressor - 6 mg ofNaCL: Isotonicity ofthe solution - 0.5 mg of sodium (meta) bisulfatc: Antioxidant - I mg of methylparaben: Bacteriostatic agent - Stenle Naler: A diluent to provide the volume ofsolution in a cartridge 1.8 cc of 2%o fidocaine (which is a calpule) with epinephrine 1:100,000 contains the following: - 36 mg oflidocaine: 1 8 x 20 mg - 018 rng of epinephrine: l 8 x 0l mg - 10'8 )ng of Nacl: 18x6mg Note; Methylparabcn is no longer included ln ,ingt.-rr. o*ot cartridges oi local anes- thetic: however. it rs lbund inALL multidose - .90 mg ofsodium {meta) bisulfate: 1 8 x 0 5 - LI mg of methylparaben I .fi x I mg - sterile watcr "i.i, "fIni".,.Uf. a-*,

Match the term on the left with the correct meaning on the right. Apnea Hypercapnia Hypocapnia Dyspnea Hyperpnea Respiratory arrest Hyperventilation Hypoventilation Below normal CO2 in arterial blood Increase in depth ofrespiration An increase in both rate and depth ofrespiration Permanent cessation of breathing (arless corrected) Transient cessation or absence of brealhino Excess CO2 in arterial blood A reduced rate and depth ofrespiration The unpleasant sensation ofdifficulty in breathing

1. Hyperventilation results in the loss of carbon dloxrde (CO) from the blood :aotes 0+pocqpnia), thereby causing a decrease in blood pressure and sometimes fainting. 2. Hypoventitation results in an increased level of carbon dioxide blood (hypercopnia). J. The respiratory rate is l0-20 breaths/min in normal adults and 44 breaths/min in infants. A respiratory rate of rate ,1. < lO/min is bradypnea. >20lmin lCO/ is considered tachypnea, and a respiratory Kussmaul breathing is an increase in both rate and depth of respiration and is synonymous with hyperventilation. 5. Cheyne-Stokes breathing is altemating hyperpnea, shallow respiration, and apnea. Children and the elderly normally show this pattern in sleep. In normal adults, causes of this pattem of breathing include heart failure, uremia, drug-in- duced respiratory depression, and brain damage. 6. Stridor is a high-pitched respiratory sound, such as the inspiratory sound heard often in acute larvnseal obstruction.

For local anesthetics for every 1% solution there is 0.10 mg/ml of anesthetic I mg/ml of anesthetic 10 mg/ml of anesthetic 100 mg/ml ofanesthetic

10 mg/ml of anesthetic For local anesthetics, for every 1o% solution there is l0 mg/ml. Therefore: To calculate the amount, in milligrams, ofany anesthetic and vasoconstrictor in a Total milligrams = 7o ofthe solution x l0 x total milliliters For vascoconstriction, for every I :100,000 there is 0.01 mg/ml-. Thereforc' Total milligrams = ratio x total milliters

Patients with a fasting plasma glucose level higher than ? or a random plasma glucose greater than ? have diabetes mellitus 50 mg/dl, 125 mg/dL 75 mg/dl, 150 mg/dl 100 mg/dl, 175 mgldL 126 mg/dL, 200 mg/dl

126 mg/dL, 200 mg/dl Diabetes Mellitus is an absolute or relative insulin insulficiency caused either by a low output of insulin from the pancreas or by unresponsiveness of peripheral tissues to insulin. Diabetes is the leading cause of blindness, end-stagc renal disease, and non-traumatic limb amputation in the Unired States. Diabctes increases risk for cardiovascular, cerebral, and peripheral vascular disease. \lanl patients \rith diabetes mellitus have no symptoms, and the diagnosis is made because ofab- nomral blood glucose lcvels detected on a routine screening. Some patients may develop polydip- sia. poll uria. polyphagia, and weight loss. In patients with severe insulin dcficiency, developmcnt ofketoacidosis may cause nausea, vomiting, lethargy, confusion, and coma. The major concem for the dentist treating a patient who has diabetes mellitus is hypoglycemia. S) mptoms of hypoglycernia: weakness, nervousness, excessive sweating, tremulousness, and palpitations. The symptoms may progress from confusion and agitation to seizures and coma without rntervenhon. ,'- - -.-,. L The treatment ofchoice for hypoglycemia in a conscious diabetic is the administra- :Notcdl tion of an oral carbohydrate (packets of table sugdr, orunge :fu$ candy bars, etc.) iuice, 2. The treatment ofchoice for hypoglycernia in an unconscious diabctic patient: EMS should bc contacted. Then I mg ofglucagon can be injected lM, or 50 ml of 50% glu- cose solution can be given by rapid IV infusion. The glucagon injection should restore the patient to a conscious state within 15 minutes; then some form oforal sugar can be glvcn. 3. People with well-controlled diabetes are no more susceptible to infections than people without diabetes, but they have more di{Iiculty containing infections (this is caused hy dltercd leukocyte function). 4. Patients who take insulin daily and check their urine regularly for the sugar and ke- toncs (controlletl diabel/., usually can be treated in the nomal manner without additional drugs or diet alterations. lmportant: Ifany doubt exists as to the patient's medical status, consultation with the patient's physician is indicated. Do not assume anything!

An incislonal biopsy is indicated for which ofthe followlng lesions? A 0.5 cm papillary fibroma ofthe gingiva A 2.0 cm exostosis ofthe hard palate A 2.0 cm area ofFordyce's disease ofthe cheek A 3.0 cm hemangioma ofthe tongue A 3.0 cm area of leukoplakia ofthe soft palate

A 3.0 cm area of leukoplakia ofthe soft palate Leukoplakia is a premalignant lesion. This means that ifleft untreated, some ofthe lesions progress to carcinoma. It is because of this chance of malignant transformation that all leukoplakias should be biopsied. Biops] Technique and Surgical Principles: . Anesthesia: Block local anesthetic techniques are employed when possible; ifnot, infiltration may be used but the solution should bc injcctcd at lcast I cm away from the lesion . . Tissue stabilization: Use fingers or clamps Hemostasis: Cauze compresses volume suction device . . . Idcision: Sharp scalpel (dvol righ speed suction) or gatze-wrappcd suction tip on a low- Extent oftissue: Obtain some normal tissue adjacent to lesion ifpossible Handling of tissue: Use a traction suture through the specimen, not tissue forceps to avoid specimen trauma. Traction sutures can also mark a point on the specimen so that the lesion can be oriented should thcrc bc a positive margin. . Specimen care: Alter removal, the tissue should be immediately placed in l07o formalin solution that is at least 20 timcs thc volume ofthe surgical specimen. Note: No othcr solution is acceptable. . wound management: Requires either a pimary closve (prefe,"d6l-r, or placement ofperiodontal drcssings in cascs ofgingival or palatal biopsies where secondary hcaling will be necessary . Recordsi A Biopsy Data Sheet should be accurately filled out The Method ofTissue Removal Varies Among the Type of Biopsies: l.ln a needle (percutareo&t biopsy, the tissuc samplc is simply obtained by use ofa s)nnge. A nee- dlc is passed into the tissue to be biopsied, and cells arc removcd through the needle. 2. In an open biopsy, an incision is made in the skin. the organ is exposed, and a tissue samplc is taken. 3. A closed biopsy involves a much smaller incision than open biopsy. The small incision is made to allow insertion ofa visualization device, which can guide the physician to the appropdate area to take the sample.

How long should one wait before obtaining a biopsy of an oral ulcer 4 days 7 days 14 days 30 days

14 days Almost all oral ulcers caused by trauma will heal within 14 days. Therefore, any ulcer that is present for 2 weeks or more should b€ biopsied. Biopsy is also indicated in the following instances: . Pigmented lesions (black/bown) . . When tissu€ is associated with paresthesia, this is often an ominous sign lfa lesion suddenly enlarges, it should be biopsied Note: Always aspirate a central bone lesion to rule out a vascular lesion. Ifa lesion seems compressible, pulsatile, blue, or a bruit is heard, beware ofa vascular lesion and biopsy only under a controlled hospital setting. ,- - . ,. .,'Notcsl-; ;ri*t; *** A stethoscope is used to listen for a bruit. l. When the entire tumor is removed, it is called an excisional biopsy technique. lf only a psrtion ofthe tumor is removed, it is called an incisional biopsy technique. 2. Brush biopsies are not recommended due to the number of false positives. 3. After removal, the tissr.re should be immediately placed in l07o formalin solution (4okformaldehyde)that is at least 20 times the volume ofthe surgical specimen. The tissue must be totally immersed in the solution, and care should be taken to be sure that the tissue has not become lodged on the wall of the container above the level of formalin. 4. A negative incisional biopsy report ofa highly suspicious oral lesion suggests that another biopsy specimen is necessary in view ofthe clinical impressions. The key is a highly suspicious oral lesion. Tissue samplings should be obtained from multiple sites ofthe lesion. Important: Unlike the more common ry?es oforal ulcers, malignant lesions are usually pain- 1ess, growing and do not heal spontaneously. Consequentl% biopsy ofany ulcer that is present in the mouth for more than 2 weeks is mandatorv.

A normal platelet count is 15,000 - 45,000/mm3 75,000 - 100,000/mm3 150,000 - 450,000/mm3 450,000 - 600,000/mm3

150,000 - 450,000/mm3 Thrombocytopenia is defined as a count of<150,000/mmr. Intraoperative bleeding can be severe with counts of 40,000-70,000/mm3, and spontaneous bleeding usually occurs at counts <20,000/mmr. minimal recommended platelet count beforc surgery is 75,000/mmr. L The minimal acceptable value for the hematocrit is 30D% for elective surgery. 2. Nomal values for coagulation: . . . Tcmplate bleeding time Prothrombin time (PT) : I to 9 minutes = 1l to 16 s€conds Partial thromboplastin time (PTT) 32-36 e/dL (comparcd to nonnal control) = activated, 32-46 seconds fcoupared to norual lmportant: PT rvill be increased by warfarin, vitamin K deficiency, fat malabsorption, livcr disease, DIC, and, artificially, increase toumiquet time. Warfarin blocks vitamin K use, whereas broad-spectrum antjbiotics elevate PT by killing normal bowel flora, which decreases vitamin K absorption. Heparin in high doses also will increase PT by altering factor X. FFP (fresh frozen plasma) 'rtill reverse warfa.in effects immediately.

A full E cyclinder of oxygen contains 150 L at a pressure of2000 psi 300 L at a pressure of2000 psi 600 L at a pressure of2000 psi 750 L at a pressure of2000 psi

600 L at a pressure of2000 psi Nitrous oxide: . . . . . . ls a colorless, nonirritating gas with a pleasant, mild odor and taste Has a blood,/gas partition coe{Iicient of 0.47 and is thus poorly soluble in blood ls excreted unchanged by the lungs ls the oldest gaseous anesthetic in use today ls the only inorganic substance used as an anesthetic As a general anesthetic, the only disadvantage is its lack ofpotency l. Nitrous oxide should be stored under pressure in steel cylinders painted blue. 2. Oxygen is stored in green tanks. 3. A full E cylinder ofoxygen contains approximately 600 L at a prcssure of2000 psi. 4. At 2 L/min, a full E cylinder will deliver oxygen for approximately 300 min, or 5 hrs.mportant: Oxygen supplementation should be avoided or used with extreme caution in patients rvith severe COPD. These patients have an increased incidence ofpulmonary bullae or blebs (combined alveoft). Because ofnitrous oxide's low blood solubiliry, it can increase the r olume and pressure ofthese lung defects, which could create an increased risk ofbarotrauma and pneumothorax.

The pH of normal tissue is ? and the pH of an inflamed area is ? 9.0;3to4 7.4;5to6 3.6;8to9 8.0;2to3

7.4;5to6 It is well known that the pH of a local anesthetic solution fdrd lre pH ofthe tissue into which it is in- jected) greatly influences its nerve-blocking action. Acidification oftissue decreases local anesthetic ef- fectiveness. Inadequate anesthesia results when local anesthetics are injected into inflamed or infected areas. Local anesthctics containing epinephrine or othcr vasopressors are acidifted by the manufacturer to inhibit the oxidation ofthe vasoprcssor. The pH ofsolutions without epinephrine is about 5.5; epinephrine-containing solutions have a pH of about 3.3. Note: Increasing pH (alkalinization) of a local anesthetic solution speeds the onset of its action, increases its clinical effectiveness, and makes its injection more comfortable. The two factors involved in the action ofa local anesthetic are diffusion ofthe drug through the nerve sheath and binding at the receptor site in the ion channel. Local anesthetics exist in ionized (cation) a d non-ionized fbare) ized (bd.re) portion forms, the proportions ofwhich vary with the pH ofthe environment. The non-ion- js the form that is capable ofdiffusing across nerve membranes and blocking sodium cha[nels.

The gold standard test for primary adrenal failure is the: Blood glucose test ACTH stimulation test Serum creatinine level BUN test

ACTH stimulation test The ACTH stimulation test is performed to examine the response ofthe adrenal gland to an exogenously administered dose ofACTH. Normal patients have a doubling ofthe serum cortisol level after a dose of ACTH. The serum cortisol level should rise to prg dL ifthere is adequate adrenal function. Art inadequate response suggests adrenal gland hrpofirnction. Note: Cosyntropin renal gland and its ACTH receptors. (Cottosyz) is an ACTH analogue that stimulates the ad- About 20 mg of hydrocortisone is secreted by the adrenal cortex daily. During stress the cortex can increase the output to 200 rng daily. Rem€mber: Patients taking steroids or people with disease ofthe adrenals will have decreased ability to produce more glucocorticoids (hydrocortisone) in times of stress tractions). The reason for this is as follows: Secretion ofglucocorticoids is stimulated by ACTH, a hormone produced in the anterior pituitary. The pituitary responds to stress by increasing ACTH output and therefore glu- cocorticoid production increases. A relative lack ofglucocorticoids will also increase out- put ofACTH. An overabundance ofcirculating systemic steroids will inhibit production ofACTH. Patients on large doses ofsteroids repress ACTH production which leads to atroohv of adrenal cortex.

Which cranial nerve innervates the lateral rectus muscle Olfactory (CN I) Oculomotor (CN III) . Abducens (CN VI) Trochlear (CN IV) Optic (CN II)

Abducens (CN VI) Importanti Cranial nerves llI (oculomolor), Vll (facial),lX and X all have parasympathetic activity.

Which cranial nerve provides motor innervation to the sternocleidomastoid and trapezius rnuscles? Glossopharyngeal (CN IX) Vagus (CN X) Accessory (CNXI) Hypoglossal (CNXII)

Accessory (CNXI)

Type 2 diabetes mellitus Was formally known as insulin-dependent diabetes Patients have little or no insulin secretion capacity Symptoms appear abruptly and include polyuria, polydipsia, polyphagia, and weight loss Accounts for 90% ofall cases ofclinical diabetes

Accounts for 90% ofall cases ofclinical diabetes Diabet€s is the most common pancreatic endocrine disorder It is a metabolic disease involving mostly carbohydrat€s fglucosel and lipids. It is caused by absolute deficiency of insulin (r,pe 1) or resistance of insulin's action in the peripheral tissues (Type 2). The classic triad of symptoms includes polydipsia, polyuria, and polyphagia.

Which of the following drugs would be best given to a patient with a history of gastric ulcers Aspirin Ibuprofen Acetaminophen Naproxen

Acetaminophen Acetaminophen (Tylenol) is the only over-the-counter non-antiinflammatory analgesic commonly available in the USA. It is a weak cyclooxygenase inhibitor in peripheral tis- sues. thus accounting for its lack of antiinflammatory effect. It may be a more effective inhibitor ofprostaglandin synthesis in the CNS, resulting in analgesic and antipyretic action. Acetaminophen does not produce gastric ulceration like aspirin does. The combination ofacetaminophen and propoxyphene (called Darvocet-N or Wygesic) is used to treat moderate to severe pain due to dental procedures. \ote: Propoxyphene (D&rvon) is an oral slmthetic opioid analgesic structurally similar to methadone. Darvon compound-65 is a combination of aspirin, caffeine, and propoxyphene. , --.. l. Acetaminophen does not affect clotting time as does aspirin 1Not5l1 h6vs significant antiplatelet effects. It is effective for the same indications as in- @;if termediate-dose aspirin. It is therefore useful as an aspirin substitute, especially in children with viral infections (who are at a riskfor Reye s syndrome iJ they take aspirin). 2. Aspirin is an anti-inflammatory antiplretic and analgesic that is used to relieve headaches,toothaches, minor aches and pains, and to reduce fever The GI tract rapidly absorbs it. 3.Talwin compound combines the strong analgesic properties ofpentazocine and the analgesic, anti-inflammatory and fever-reducing properties ofaspirin. It is used for the relief of moderate pain. It does not produce euphoria. 4. The most appropriate time to administer the initial dose of an analgesic to control postoperative pain is before the effect ofthe local anesthetic wears off. 5. Remember: the following analgesics should be avoided in patients with renal disease: aspirin, acetaminophen, NSAIDs, meperidine and morphine.

All of the following are contraindications to tooth extraction except one Acute pericomitis . Acute dentoalveolar abscess End-stage renal disease Acute infectious stomatitis

Acute dentoalveolar abscess An acute dentoalveolar abscess should not be a contmindication to extraction. It has been shosn that these infections can rcsolve very quickly when the affected tooth is removed. How- ever. it may be difiicult to extract such a tooth, either because the patient is unable to open suf- ficiently wide enough or because adequate local anesthesia cannot be obtained. There are fe\r,tlue contraindications to the extraction ofteeth. Note: In some instances, the pa- rients' health may be so compromised that they cannot withstand the surgical procedue. Examples of contraindications include: . . . . . . End-stage renal disease Ser ere uncontrolled metabolic diseases -A.d\ anced cardiac conditions (unstable angina) (i.e., uncontolletl diabetes mellitus) Patients \\'ith leukemia and lymphoma should be treated before extraction ofteeth Parients \r'ith hemophilia or platelet disorders should be treated before extruction ofteeth Parients with a history ofhead and neck cancer need to be treated with care because even minor surgery can lead to osteoradionecrosis, Not€: These patients are often treated with hy- perbaric oxygen therapy pdor to dental sugery. . Pericomitis: infection ofthe soft tissues around a partially erupted mandibular third molar \ote: This infection should be treated p or to removal of the maxillary third molar . . Acute infectious stomatitis and malignant disease are relative contraindications Patients being treated with tV bisphosphonates increases the risk ofosteoradionecrosis of the Jaw Note: Causes ofexcessive bleeding after dental extractions include; injury to the inferior alveolar artery during extraction ofa mandibular tooth (usually the third mola/), a muscular arte- patients who are on warfarix or drugs.for platelet ixhibition, pqtients vrho have hemophilia or von Wlle- riolar bleed from a flap procedure, or bleeding related to the patient's history [.e., brand's disease, or who have chronic liver insfficiency).

Malignant hyperthermia (MH) is a pharmacogenetic disorder in which a genetic variant in the individual alters that person's response to certain drugs. The major clinical characteristics of MH include all of the following EXCTPT one. Which one is the EXCEPTION. Rigidity Fever Hypermetabolism Myoglobinuria Alkalosis

Alkalosis MH is a hypermetabolic state involving skeletal muscle that is precipitated by certain anesthetic agents in genetically susceptible individuals. The incidence ofMH is all patients who are exposed to anesthetic agents. Inhalation anesthetic drugs that are krown to trigger MH include halothane, enflurane, isoflurane, desflurane, and sevoflurane. Depolarizing neurornuscular blockade agents that can trigger MH include succinylcholine, decamethonium, and suKamethonium. Classic MH most often manifests in the operating room, but it can also occur within the first few hours ofrecovery from anesthesia. When exposed to inlalational anesthetics, muscle metabolism increases, and a series ofsigns and symptoms appear, which if left untreated can lead to death. The earliest findings are an increased production olcarbon dioxide and signs of increased s),mpathetic nervous sys- tem activity. Acute clinical manifestations of MH include tachycardia, tach)?nea, unstable blood pres- sure, cyanosis, respiratory and metabolic acidosis, fever, muscle rigidity, and death. Mortality ranges from 6 3%o to 73o/o.Il vsually occurs in apparently healthy children and young adults at an average age of 2l years. When MH is diagnosed early and treated promptly, the mortality rate should be near zero. Whenever anesthesia is administered, dantrolene should be readily available as well as a protocol for managemeni of MH (100% oxygen, cooling procedures, and the correction of acidosis and hyperkalemia). Dantrolene is, at the moment, the only known drug that lreats MH. It impairs calcium-dependent muscle contraction and controls hypermetabo- lism manifestations.

All of the following are ways to eliminate deda space except one Close the wound in layers to minimize the postoperative void Apply pressure dressings Use drains to remove any bleeding that accumulates Allow the void to fill with blood so that a blood clot will form

Allow the void to fill with blood so that a blood clot will form Dead space in a wound is any area that remains devoid of tissue after closure of the wound. It is created by either removing tissues in the depths of a wound or by not reapproximating tissue planes during closure. Dead space in a wound usually fills in with blood which creates a hematoma with a high potential for infection. This is more likely to happen in closed wound incisions or in an open wound that has closed over at the top too quickly, leaving "dead space" open underneath. Some of these may resolve them- selves, but most need to have the fluid drained and the "dead space" needs to be closed, either by deep suturing or by re-opening the top ofthe wound and packing until it heals from the bottom up. Ways in which you can eliminate dead space: . . . . Close the wound in layers to minimize the postoperative void Apply pressure dressings Use drains to remove any bleeding that accumulates Place packing into the void until bleeding has stopped Important: Infections are uncommon in healthy patients. However, whenever a mu- coperiosteal flap is elevated for a surgical extraction, there is a possibility for a subpe- riosteal abscess. Thus, all surgical flaps should be irrigated liberally prior to closing $ ith sutures. Note: The treatment for a subperiosteal abscess is drainage of the abscess and antibiotic treatment.

For maxillary extractions the upper jaw of the patient should be Below the height ofthe operator's shoulder Above the height of the operator's shoulder At the same height ofthe operator's shoulder It makes no difference where the patient's upper jaw is in relation to the operators shoulder

At the same height ofthe operator's shoulder The chair usually has to be repositioned to be satisfactory for exodontics. For mandibular extractions, the patient should be positioned so that the occlusal plane ofthe mandibular arch is parallel to the floor when the mouth is opened. The chair should be as low as possible. For maxillary extractions, the upperjaw ofthe patient should be at the height of the operator's shoulder These positions allow the upper arm to hang loosely from the shoulder girdle and obviate the fatigue associated with holding the shoulders in an un- nanrrally high position during the course ofthe day. The low positions allow lhe operator to bring the back and leg muscles into the operation to assist the arm. The chair can be tipped backward slightly for maxillary extractions. The fingers ofthe left hand (for a right-handed dentist) serye lo: . . . . . Retract the soft tissue Provide the operator with sensory stimuli for the detection ofexpansion ofthe alveo- lar plate and root movement under the plate Help guide the forceps into place on the tooth Protect teeth in the oppositejaw from accidental contact with the back ofthe forceps Support the mandible while performing mandibular extractions Remember: recommended sequence of extraction: . . Maxillary teeth before mandibular teeth Posterior teetlr before anterior teeth

Diminished volume affecting all or part of our lung is called Bronchiectasis Atelectasis Pneumothorax Pneumonia

Atelectasis Atelectasis occurs when mucus or a foreign object obstructs airflow in a mainstem bronchus causing collapse ofthe affected lung tissue into an airless state. It typically occurs 36 hours postoperatively and presents with mild dyspnea, low-grade fever, and hy- poxia. Note: Prolonged atelectasis can lead to pneumonia' The treatment of postoperative atelectasis is aimed at expansion of the lung, and, for most patients, incentive spirometry @ncouraging the patient to take long, slow, deep breaths) is adequate. However, in patients with severe atelectasis, endotracheal suction and even bronchoscopy may be warranted. Pneumothorax occurs when air leaks into the pleural space causing the lung to recoil from the chest wall. In an awake patient, a pneumothorax typically presents with dyspnea, chest pain, absence ofbreath sounds on the affected side, and evidence ofpneumothorax on a chest x-ray. Tracheal deviation may be present. The objective of treatment for a pneumothorax is to remove the air lrom the pleural space, allowing the lung to re-expand. In an emergency, a small needle (such as a stan- dard intravenous needle) may be placed into the chest cavity through the ribs to relieve the excessive pressure. The definitive treatment is a chest tube, a large plastic tube that is inserted through the chest wall between the ribs to remove the air completely. - . 1. Pneumonitis (inflammation of the lung) and atelectasis are two of the most roleg.' 66mmsn causes of fever in a patient who has had general anesthesia. la;*;Jl 2. Th" nausea. -ost common post-op complication ofoutpatient general anesthesia is

The facial nerve carries Efferent components only . Afferent components only Both efferent and afferent components

Both efferent and afferent components The facial nerve leaves the cranial cavity by passing through the intemal acoustic meatus, which leads to the facial canal inside the temporal bone. Finally, the nerve exits the skr.rll by way of rhe stylomasloid foramen of the temporal bone. Note: lfyou cut the facial nerve just after its exit from the sylomastoid foramen, it would cause a loss of innewation to the muscles of facial expression. The facial nerve carries an efferent component for the muscles of facial expression and for the preganglionic parasympathetic innervation ofthe lacrimal gland (relaying in the ptery- gopalatine ganglion) and submandibular and sublingual glands (relar-ing in the submandibular gangliott). The afferent component serves a tiny patch of skin behind the ear, taste sensation, and the body ofthe tongue. Clinical information: l. Bell's palsy: involves unilateral facial paralysis with no known cause, except that there is a loss ofexcitability ofthe involved facial nerve. The onset ofthis paralysis is abrupt, and most symptoms reach their peak in 2 days. One theory of its cause is that the facial nerve becornes inflamed within the temporal bone, possibly with a viral etiology. L Trigeminal neurzlgia (tic douloureLLr): also has no known cause but involves the affereni nen:es of the trigeminal nerve. It usually involves the maxillary or mandibular nerve branches but not the ophthalmic branch. One theory is that this lesion is caused by pressure on ihe sensory root ofthe trigeminal ganglion by area blood vessels. Clinically, the patient feels excruciating short-term pain f/ic/ when facial trigger zones are touched or when speak- ing or masticating, setting offassociated briefmuscle spasms in the area. The right side of the tace is affected more commonly than the left. It is more common in females. Carba- mazepite (Tegretol) is still the mainstay oftreatment.

There are no contraindications for the use of nitrous oxide sedation in asthmatic patients nitrous oxide is usually beneficial for those patients Because anxiety is a stimulus for an asthma attack The first stalement is true, the second is false The first statement is false, the second statement is true Both statements are true Both statements are false

Both statements are true \ausea and vomiting are the most conmon adverse effects ofnitrous oxide sedation, oc- curring in l% to l0% of patients. Fasting is not required for patients undergoing nitrous oride sedation. The practitioner, however, may recontmend that only a light meal be con- sumed in the 2 hours prior to the administration of nitrous oxide. Diffusion hypoxia can occur as a result ofrapid release ofnitrous oxide from the blood stream into the alveoli, thereby diluting the concentration ofoxygen. This may lead to headache and disorienta- tion and can be avoided by administering 1007o oxygen after nitrous oxide has been discontinued. Remember: The most common complication associated with nitrous oxide sedation is a behavioral problen (laughing, giddy). Note: Some literature states that nitrous oxide is acceptable for the pregnant patient, however, from a risk management point it may be prudent not to use nitrous oxide on any pregnant patlent. Administration ofvolatile an€sthetics (desflurane, enflurane, halothQne, isoJlurane, and sevo.flurane) is not a concern for COPD patients. All volatile anesthetics are bron- chodilators and, therefore, are beneficial to patients with COPD (asthmatic bronchitis, emphysema, sand chronic bronchitis). Important: Sedation with nitrous oxide should be aYoided in patients with COPD.

In general shock is characterized by all except one Increased vascular resistance Bradycardia Myocardial ischemia Mental status changes Adrenergic response

Bradycardia (shock is tachycardia) The term shock denotes a clinical slrldrome in which there is inadequate cellular perfusion and inadequate oxygen delivery for the metabolic demands ofthe tissues. Important: Reduced cardiac output is the main factor in all tlpes ofshock. In eeneral. shock is characterized bv: ."lncreased vascular resistance: co61 mottled skin, oliguria . . . Tachycardia Adrenergic response: diaphoresis, anxiety, vomiting, diarrhea \l]'ocardial ischemia . \lental status changes The stages ofshock include: -l) Compensatory -postedor, (early) stage: compensatory mechanisms (fu- credsed heart rdte and peripheral resistazce) maintain perfusion to vital organs, 2) Progres- sire stage: metabolic acidosis occurs (compensatoty 3t lrrercrsible mechanisms are no longer adequate), (refractot)) stqge). organ damage, survival is not possible. \Iajor Categories of Shock: . Hlpovolemic shock is produced by a reduction in blood volume. Cardiac output will be lou,due to inadequate left ventricular filling. Causes include severe hemonhage, dehydra- tion. vomiting, diarrhea, and fluid loss fiorn bums. . Cardiogenic shock is circulatory collapse resulting from pump failure ofthe left ventri- cle. most often caused by massive myocardial infarction. . Septic shock is due to severe infection. Causes include the endotoxin from gram-nega- tive bacte a. . . Neurogenic shock results from severe injury or trauma to the CNS. Anaphylactic shock occurs with severe allergic reaction.

Atropine and scopalamine have similar pharmacological effects. Which of the following actions does only scopalamine have? Reduction of salivation Prevention of cardiac slowing during general anesthesia CNS depression Mydriasis Cycloplegia

CNS depression The cholinergic blocking (anticholinergic) drtgs competitively inhibit the action of acetylcholine at parasympathetic postganglionic neuroeffector sites. The principal drugs in this category are atropine and scopolamine, which are useful in dentistry as agents to control salivary secretion and as preanesthetic medication. The desirable clinical effects ofthe anticholinergics are mydriasis, antispasmodic actions, and reduction in gastric and salivary secretions. The pharmacologic actions ofatropine and scopolamine are similar in many respects. At- ropine in the usual dose employed in dentistry does not show a CNS response. Scopo- lamine, however, has a depressant effect on the CNS, which accounts for its usefulness as a preanesthetic agent and perhaps its use in motion sickness in several over-the-counter preparations. Both drugs will reduce salivary flow and in large doses block the cardiac- slowing effect ofthe vagus nerve. Anticholinergic drugs should be used with considerable caution in patients with cardio- vascular disease and are contraindicated in patients with glaucoma, prostate hypertrophy, and intestinal obstruction. Side effects are common with the anticholinergic drugs and include blurred vision, tachy- cardia. urinary retention, constipation, decreased salivation, sweating, and dry skin. \ote: Atropine and scopolamine are also extremely useful in therapy and examination of the eye. These drugs produce dilation (nydriasis) and paralysis of accommodation for distance vision and bght (cltcloplegia). Such effects are generally long lasting and can also be manifested by larger systemic doses ofthe drugs.

Which of the following teeth could be removed without pain after administration of an inferior alveolar or lingual nerve block All anterior teeth on the side of the injection Canine and first premolar on the side ofthe injection All teeth in that quadrant on the side ofthe injection Both premolars and first molar on the side of the injection

Canine and first premolar on the side ofthe injection bu need !o qive a long buccal inj€ction in orderto extract the molars and second bicuspid. For operative pro- ccdures, a long buccal iniection may not be needed for tbese teefi. The long buccal irjection anesthetizcs thc soft tissuc and periosteum buccal to the mrndibular molar tecth. Thc nccdle is insened in thc mucous mem- brane distal and buccal to the nost distal molar in lhe arch. 'fo anesthetize the lingu!l nerve: When administering an infcrio. alveolar nene block slorvly withdraw thc slringc, and whcn approximately halfits length remains within tissues, r€aspirate. Ifnegativc, dcposit a por- tion of the remaining solution /0.,1 for cxtractions- ,r// to anesthetize the lingual nerve. Incisors may need local infiliration Other Techniqucs of I\landibular 4nertheria: . Mental nen'e block: This nerve block is used whcn buccal sofFtissue anesthesia is n€cessary anterior to the mcntal tbramen (around the second premolar) ro the midline and skin of the lower lip and chin. The needle is insened in mucobuccal fold tt orjust antcrior lo thc mental foramen. Ttrget area: mental ncne as it exits thc mcntal foftfien . (usuall! located berween the apices (t the-lirst and second Vazirani-Alkinosi closed-mouth mandibular block: although this tcchnique can be used *'henever mandibular anesthesia is desired, its primary indication remains those situations in which limited mandibufar opeDing (i.e., patienls r\'ilh r/lrrrrsl precludes the use ofolher mandibular lechniques. Nerves anes- thetized: inferior alveoiat incisive, mcntal. lingual, mylohyoid nen'es. Are! of needle insertion: soft tissue overlying the medial /1lrgl/d/) at the height ofthe mucogingival prcnblars). border ofthe mandibular ramus dirccily adjacent to the maxillary tuberosity junction ad.lacent to the maxillary third molar. Not€: The injeclion is per- formed blindly becausc no bony endpoints exists, the needle is advanccd 25 mm into tissue (&r dn awrage- si:ed adult).'fhe distance is measured from the maxillary tuberosiry. . The Cow-Cates technique; this technique is a true mandibulirr nene block because it provides sensory anesthcsia to virtually the entire distribution ofV3 ftnferior alrcolar, lingual, n\,lob'oid. nenlal, itcis[w, auriculotenporal, ancl buccal ner|es). hs primary use is when a conlentional inferior alveolar nervc block is unsuccessful. Not€i Patient must cxtcnd his or hcr neck and open *ide for the duration ofihe technique lthe nnaie hen assunes a more.frontal position and is closer to the andibular nerw trunv. Extraoral landmarksi comcr ofmouth, tragus ofear, and intcrtragic notch Area of needle insertion: lhe needle is positioncd so that it is insened just distal 1o thc moxillary sccond molar at the height of its mesiolingual cusp. The needle is slowly advance until bone lneck ofthe concl.rle) is conlacted. The avelagc deplh ofsofF tissue penetration to bone is 25 mm. The needle tip is withdrawr I mm, aspirate, and slowly deposit solu-

Nitrous oxide works on the Peripheral Nervous System (PNS) Central Nervous System (CNS) Autonomic Nervous System (ANS)

Central Nervous System (CNS) n-itrous oxide is the only inorganic gas used by the anesthesiologist. Room air contains 2l%o oxygen; you must mak€ sure that th€ pati€nt rec€ives at least this much oxygen. The max- imun nitrous oxide limitation is 60% nitrous oxide and 40olo oxvsen. \itrous oxide is carried in the bloodstream in physical solution. There is no metabolism or degradation ofnitrous oxide in the body. It is excreted solely via the lungs, unchanged. High blood levels olnitrous oxide can be achieved quite quickly. It is non-toxic to body tissues. Tle only toxicity with the use ofnitrous oxide is the lack ofoxygen that could result from the operator's error. The gag reflex is only slightly obtunded with nitrous oxide analgesia. lt is be- lie\ ed rhat nitrous oxide has its main effects on the reticular actiyating system and the lim- bic sl'stem. \irrous oxide is a weak anesthetic. It is used to supplement inhalation agents. tt is the only in- halation anesthetic with sympathomimetic activity. It should not be used in dos€s higher than 60cb combined with 40% oxygen. It is known to diffuse into air containing spaces and to in- crease the pressure in such cavities. 100% oxygen should be administered during awakening in order to avoid diffusion hypoxia. Remember: . . The first symptom ofnitrous oxide analgesia is tingling of the hands. Nausea is the most common side effect ofnitrous oxide analgesia. .The correct total liter flow ofnitrous oxide/oxygen is determined by the amount necessary to keep the reservoir bag 1/3 to 2/3 full. MAC (minimal alveolar concentrqtioz) ofnitrous oxide is 104. MAC is the concentration of an inhaled anesthetic at I atm that prevents skeletal muscle movement's response to a painful stimulus (e.g., suryical skin incision) in 50%o of patients.

A 55-year-old male presents to your office with a long history of a productlve cough. The patient states the cough has been present for 6 months each ofthe last three years. The patient is afebrile and chest x-ray is unremsrkable. Which of the following is the most likely diagnosis? Viral pneumonia Chronic bronchitis Emphysema Asthma

Chronic bronchitis COPD is a disease due to persistent airway obstruction. Two diseases account for the bulk of the patients with COPD: €mphysema and chronic bronchitis. There is continuing debate as to \rhether this term also includes acute asthma, however as a general ru1e, it is not incft'rded as. even though it does have obstructive components to it, it is in part reversible, and is more generally considered a restrictive lung disease. ln most cases, bronchitis and emphysema occur togerher \ote: Secondary pulmonary hypertension is most often caused by COPD. Important: l. Drugs with antiplatelet activity fasplnn) should be prescribed to COPD patients with cau- tion. Hemoptysis has been reported after the use ofaspirin in patients with COPD. 2. COPD patients taking theophylline should not b€ prescribed erythromycin. Erythromycin increases the metabolism oftheophylline and may cause toxiciry.

Your 60-year-old patient presents with congestive heart failure. They note cardiac symptoms wlth mild activity but are asymptomatlc at rest. What is the functional classification of heart failure in your patient? Class I Class II Class III Class IV

Class III Class I congestive heart 1'ailure is defineu as no symproms toms with marked activity, Class Itl is symptoms with mild activity, and Class IV is symptoms at rest. Congestive heart failure (CHF) results ftom impaired pumping ability by the heart. A ventricular ejection fraction bclou, 50% is indicative ofCHF. Valvular hcart discasc, coronary artery discasc, arrhythmias, hypothyroidism, high-cardiac output syndromes, and hypertension can lcad to heart failurc. Note: Usually the left ventricle fails first, soon followed by right-sided failure. The pres€nting symptoms include dyspnea, orthopnea, paroxysmal noctumal dyspnea, fatigue, exercise intolerancc, and odema. Note: The most comnron sign of lefFsided heart failure is pulmonary edema, whcrcas righGsided heart failure causes pedal ed€ma or abdominal swelling. Pharmacologic therapy: goals are to contol fluid retention, control neurohormonal activation, and control sYmDtoms. . . Diuretic; fe.g., ACE inhibitors Lasix, Aldactone, Zaroxolyn), are uscd to control fluid retention fe.g., , Class II is symp- Captopril, Lisinopril), which interfere with the renin-angiotensin sys- ten, are required ofall paticnts with cardiac failure unlcss contraindicated . Vasodilators, including hydralazine and nitrates, are used when the use ofACE inhibitors is not oossible . Beta blockers feg. , Car-vedilol, Bisoprolol, Metopt'olol, lten o/of, should be used in patients with left ventricular dysfunction, unless contmindicated . Digitalis can improve symptoms and exercise tolerance by increasing cardiac contractility . . Other medications include oxygen and morphine Aspirin, NSAIDs, and calcium channel blockers should be avoided Patient treatment and dental managemcnt considerations: . . . Prolonged rest, administration ofoxygen Digitalis (patients are prone to nousea and vomiting) Diuretics/vasodilators (patients are prone to orlhostqtic hlpotension: a\oid excessive epi- nephrine/ . Dicumarol (patients may have bleeding problem,/

Patients with glucocorticoid hypersecretion have Ectopic ACTH Syndrome MENS I Cushing's syndrome Addison's disease

Cushing's syndrome Cushing syndrome is a hormonal disorder caused by prolonged exposure ofthe body's tis- sues to high levels ofthe hormone cortisol. This results in characteristic changes in body hiatus including moon facies, truncal obesity, muscular wasting, and hirsutism. Some- times called "hypercortisolism," it is relatively rare and most commonly affects adults aged 20 to 50. The femaleto-male incidence ratio is approximately 5:1. Patients with Cushing's syndrome are often h)?ertensive because offluid retention. Longterm glucocorticoid excess can result in decreased collagen production, a tendency to bruise easily, poor wound healing, and osteoporosis. They are often at increased risk for infection. Laboratory snrdies may reveal increased blood glucose levels because ofinterference with carbohydrate metabolism, and examination of the peripheral blood smear may demon- strate slight decrease in eosinophil and lymphocyte counts. Important: The patient's cardiovascular status must be evaluated and treated if necessary prior to surgery. Note: The most common cause ofCushing's syndrome is a tumor in the pituitary ofthe hloothalamus.

Volatile liquids require a vaporizer for inhalation administration. Which one additionally requires a heating component to allow delivery at room temperature? Enflurane Halothane Sevoflurane Desflurane Isoflurane

Desflurane lnhalation anesthetics are substances that are brought into the body via the lungs and are distributed with the blood into the different tissues. The main target ofinhalation anesthetics (or so-cqlled yolatile anesthetics.) is the brain. Currently used inhalation anesthetics include five volatile liquids enflurane, halothane, isoflurane, sevoflurane, desflurane, and or'e gas (nitrous oxide). -fhe volattle liquids require a vaporizer for inhalational administration. The desflurane vaporizer has a heating component to allow delivery at room temperature. Some inhalation agents have an unpleasant odor and may irritate the respiratory tract. This irritation may cause coughing and muscle spasms in the voice box, or larynx (lary-ngospasm), or in the bronchial tubes in the lungs (bronchospasm). Sevoflurane is less irritating to the air- way than the othen and is preferred for inducing anesthesia in children. Important: All the potent inhalation agents are capable oftriggering malignant hyperthermia LllH), a rare rnherrted disorder that is potentiallv fatal. -{dministration ofan inhalation anesthetic is usually preceded by intravenous or intramus- cular administration ofa short acting sedative hypnotic drug, often abarbiturate (Thiopental). The procedure almost always requires endotracheal intubation. \ot€ l. Administration of volatile anesthetics is not a concem for COPD patients. All volatile anesthetics are bronchodilators and therefore are beneficial to patients with COPD. 2. Volatile anesthetics depress the cardiovascular system, and this depression results in a reduced mean arterial pressue. 3. Desflurane, isoflulane, and sevoflurane are potent vasodilators.

A tall, thin patient presents to your olnce with shortness of breath. On examination you note the patient is breathing through his expiratory phase is prolonged and lung sounds are distant. Which of the following is the most likely diagnosis? Asthma Bronchiectasis Cystic fibrosis Emphysema

Emphysema The emphysema or "pink blood vessels, puffer" patient is typically thin and presents with dyspnea, pursed- lip breathing and pink skin color, Arterial blood gases reveal hypoxia and hlpercapnia. Em- physema is defined as destructive changes to the alveoli walls and enlargement ofair spaces. Ir affects the lung parcnchyma distal to terminal bronchioles. Cigarette smoking is major risk faclor (increases risk by 10 to 30 times otter nonsmokers). Note: Alpha- l -antitrypsin defi- ciency should be suspected in patients who develop emphysema in their late 30s. Bronchiectasis: abnormal dilatation ofthe large conducting pathways, due to congenital struc- tural abnormalities or acquired processes. Congenital causes include cystic fibrosis and alpha- l-antitrypsin deficiency. Acquired processes include viral and bacterial infections, foreign bodies, and tumors. The major symptom is a cough, which is daily and productive with purulent sputum. Hemoptysis may accompany the cough. As disease progresses, exercise intoler- ance and dyspnea develop. Cystic librosis: an autosomal recessive disease and most common lethal inherited disease in American whites. Most patients are diagnosed in the preteen years. It is due to a defect in cys- tic fibrosis transmembrane conductance regulator. S).mptoms are due to development ofthick secretions that block the airways and ductal system in other organs (usually pancreas and /1rc,.r. Common s),rnptoms include chronic cough with sputum production and dyspnea. Remember: Patients with chronic bronchitis (or any COPD) can have difficulty during oral surgery Many of these patients depend on maintaining an updght posture to breathe adequately. They frequently experience difficulty breathing ifplaced in an almost supine position or ifplaced on high-flow nasal oxygen. Important: Patients with chronic bronchitis may be predisposed to lung cancer (bron- chogenic carcinoma).

Which of the following provides branches for the most direct blood supply to the TMJ Intemal carotid artery Extemal carotid artery Cornmon carotid artery Aorta

Extemal carotid artery The major arterial blood supply to the TMJ is derived from the superficial temporal artery and from the maxillary artery posteriorly, and from smaller masseteric, posterior deep temporal, and lateral pterygoid arteries anteriorly. The venous drainage is through a diffuse plexus around the capsule and rich venous channels that drain the retrodiscal rissue. ){ot€: The two terminal branches of the extemal carotid artery are the superficial temporal artery and the maxillary artery. The fibrous capsule of the TMJ is innervated from a large branch of the auriculotem- ofV-3).The rnterior region ofthejoint is innervated from the masseteric nerve poralrerYe (branch (also a branch of V-3) and from the posterior deep temporal nerve (a/so a bronch oJ'V-3).The sensory innervation ofthe TMJ is via the trigeminal nerve as well. The nerve fibers prirnarily follow the vascular supply and terminate as free nerve endings. Thus. the capsule, synovial tissue, and extreme periphery ofthe disc are innervated. The anicular cartilage and the central part ofthe disc contain no nerv€s. Both myelinated and nonmyelinated nerves are seen in the TMJ. The retrodiscal bilaminar zone has a rich neurovascular supply and is the source ofproprioception. Remember: Most synovial joints -paralysis have hyaline cartilage on their articular surface; how- ever, a number ofjoints, such as the stemoclavicular, acromioclavicular, and TMJs, are associated with bones that develoo from intramembranous ossification. These have fi- brocartilage articular surfaces.

The TMJ is a Arthrodialjoint Ginglymus joint Ginglymoarthrodial joint

Ginglymoarthrodial joint Because the TMJ has characteristics ofboth a hinge moarrhrodial joint and a gliding joint, it is classified as a gingly- joint. A unique feature ofthe TMJ is that it is rigidly connected to both the dentition and the contralateral TMJ. Components ofthe TMJ: . Mandibular condyle (sometines called the cowlyloid process of the mandible) - the aniculating sur- face or functioning part of the condyle is located on the superior and anterior sudaces ofthe head of the condyle. This surface is covered with a dense layer oflibrous connective tissue. . Articular fossa - this fossa is the anterior three-fourths ofthe laryer mandibular fossa. It is consid- ered to be a notr-functioning portion ofthejoint. Remember: The mandibular fossa (g/enoidfossa) is rhe remporal component ofthe TMJ; it is bounded in front by the articular eminence, and behind, b-v the tympanic part of the temporal bone, which separates it from the extemal auditory meatus. Articular eminence (also called the articular tubercle) - is aidge that extends mediolaterallyjust in fiont ofthe mandibular fossa. It is considered to be the functional portion ofthejoint. It is lined . $ ith a thick dense layer of librous connective tissue. . -A.rticular disc /a/,ro called the meniscus) - is a biconcave librocartilaginous disc interposed be- t\|een the condyle ofthe mandible and the mandibtiar (glenoid) fossa ofthe temporal bone which pro- gliding surface for the mandibular condyle, resulting in smoothjoint movement. The cenhal part is avascular and devoid ofnerv€ tissue, only the extreme periphery is slightly innervated.

A 50 year old woman wants the removal of a painful 2nd mandibulr molr. She hasnt rested for two days bc of the pain. She takes 20mg per day of prednisone for erythema multiforme. How do you treat her Have patient discontinue the Prednisone for two days prior to the extraction Give steroid supplementation and remove the tooth with local anesthesia and sedation lnstruct the palient to lake 3 grams of amoxicillin one hour prior to extraction No special treatment is necessary prior to extraction

Give steroid supplementation and remove the tooth with local anesthesia and sedation Important: The f€ar here is that the patient may not have sumcient adrenal cort€x secretion (adrenal in- sulJiciency) to withstand the stress of an €xtraction without taking additional steroids. (This holds true for any palient who has been treatedfor any disease vilh steloid therapy). Patients with adrenal insufficiency, patients on daily steroid therapy, and patients who have rccently fin- ished a couNe of stercids should receive steroid supplement for dental procedures. The concems about adrenal insufficiency should be raised on the basis ofclinicrl history. In the majority ofcases, the dentist should ask: . . Is it known that the patient's adrenal glands do not function adequately? Is the patient on chronic steroid therapy at doses ofprednisone higher than 15 mg/day? . Has the patient been on steroid therapy at doses ofprednisone higher than l5 mg/day within the last 2 weeks? *** Ifthe answer to any ofthe above questions is yes, the dentist should assume that the patient will need stress-dose steroids. G€neral guidelines for the management ofpatients on steroid therapy: . . . . . Steroid supplement in patients who can develop adrenal insulliciency Early moming appointm€nts Shoner appointrnents Minimize stress Use sedation techniques when appropriate . Modiry dental treatment plan when appropriate . The major goal in these patients is to avoid precipitation ofadrenal insufnciency Remember: Erythema multiforme is a hypersensitivity syndrome characterized by polyrnorphous eruption ofskin and mucous membranes. Macules, papules, nodules, vesicles, or bullae and target or ("bull's-eye-shaped") lesions aie seen. A sev€re form ofthis condition is known as StevensJohnson syndrome, These patients may be receiving moderate doses of syst€mic coficosteroids and therefore may be unable to withstand the stress ofan extraction. Consultation with theirphysician is absolutely nec- essary before treating these patients.

The clinical presentation of acute asthma includes all of the following except Dyspnea or tachypnea Wheezing Hypoxemia Occasionally hypercapnia Hemoptysis

Hemoptysis Asthma is a condition chamcterized by episodic reversible narrowing of the airways. The most common symptoms include episodic wheezing, cough, chest tightness, and shortness of breath. The disease can begin at any age, but about half ofpati€nts develop asthma before the age of 10. There are three basic pathophysiologic changes: (1) Airway inflammation (2) Airway obstruction and (3) Airway hlperresponsiveness lmportant: An acute asthmatic attack is best heated by administration ofsupplemental oxygen with an inhalaled beta2-adrenergic agonist (albuterol, terbutaline). lf the patient is resistant to beta agonists, theophylline should be considered. In a severe asthmatic attack that is unresponsive to the above treatment, 0.3 mg of 1;1000 epinephrine should be administered subcutaneously. Important: There are no contraindications for the use ofnitrous oxide sedation in asthmatic patients. Because anxiety is a stimulus for an asthmatic attack, nitrous oxide sedation is actually ben- eficial for these patients. Ifpatient is taking steroids, consult physician for the possible need for corticosteroid augmentation. General guidelines for the management ofpatients with asthma: . Minimize stress: short appointments, use sedation techniques (nib'ous, diozepam or olher oral a n t ianie t,v med icq t iotls . . Avoid antihistamin€s ). Minimize epinephrine \se (local anesthesid trp to 2 carpules of 226 lidocaine with 1:100,000 epinephrihe may be used) . . Avoid erythromycins and clarithromycin in patients on theophylline Be arvare ofaspirin sensitivity; there is a clinical triad ofasthma, nasal polyps, and aspirin sen- sitivity. h is inportant to be sure that the patient with asthma does not have this triad when as- pirin-containing preparations are prescribed. Status asthmaticus is the most severe clinical form ofasthma, usually requiring hospitalization, that does not respond adequately to ordinary therapeutic measures. Ifnot managed properly, chronic partial airway obstruction may lead to death from respiratory acidosis (which is p oxem i a a nd hypercapn ia).

The maxillry sinus opens into the middle metus of the nose through Frontonasal duct Bulla ethmoidalis Hiatus semilunaris Nasolacrimal duct

Hiatus semilunaris Unfortunately, this opening lies high up on the medialwall ofthe sinus, so that the sinus readily accu- mulates fluid. Sincc the frontal and anterior ethmoidal sinuses drain into the infundibulum, which in tum drains into the hiatus semilunaris, the chance that infection may spread from these sinuses into the maxillary sinus is great. 2 tlpes of sinusitisr acute and chronic: common clinical manifestations include sinus congestion, dis- charge, pressure, face pain, and headaches. Acute Sinusitis: the most common fonn ofsinusitis, typically causcd by a cold that results in inflam- mation ofthe sinus membranes, normally resolves in I to 2 weeks. Sometimes a secondary bactedal infection may seftle in the passageways after a cold; bacteria normally located in thc area pneutnnide dnd Hdeuophilus influenzae) may begin to increase, producing an acute bacterial sinusitis. Clinical signs ofacute sinusitis include . . . . . Severe pain, constant and localized Tendemess to percussion ofthe maxillary posterior teeth A mucopurulent exudate Any unusual motion orjarring accentuates the pain Tendemess over the anterior sinus wall Chronic sinusitis: an infcction ofthc sinuses that is present for longer than 1 month and requires longer duration medical therapy. Typically either chronic bacterial sinusitis or chronic noninfectious sinusitis. Chronic bacterial sinusitis is trcatcd with anttbiotics (ampicillin or auqme tin). Chronic noninfectious sinusiris often is treated with steroids (opical o/ oral) and nasal washes. Locations of sinusitis: . \Ie\illary: the most common location for sinusitis; associated with all of the common signs and s)mproms but also results in tooth pain, usually in the molar region . sphenoid: rarc, but in this location can result in problems with the pituitary gland, cavemous sinus spdrome, and meningitis . Frontal: usually associated with pain over the forehead and possibly fever . Ethmoid: potential complications include meningitis and orbital cellulitis. \ote: Thc maxillary sinus is innervated by the maxillary division of the trigeminal nerve (CN l/-2). Speciiicall-v. the ASA, PSA, and MSA nerves as well as the inliaorbital nervc.

All of the following are signs and symptoms that would suggest that your patient is dehydrated except Pale or gray skin color Dry mouth Decreased skin turgor Modified state ofconsciousness High blood pressure Rapid pulse Reduced urine output

High blood pressure (actually there is low BP) Dehydration is the loss ofwater and important blood salts like potassium (K-) and sodium (Na"). Vital organs like the kidneys, brain, and heart can't function without a certain min- imum amount of water and salt. Causes include decreased intake (ack ofwater) and. / or increased output fvomititlg, diat"rhea, Ioss ofblood, drainageJi'om burns, diabetes melli- tus, diuretic use, or a lack ofADH owing to diabetes insipidus). Initially, a patient suffering from dehydration will clinically demonstrate only dryness of the skin and mucous membranes. However, as dehydration progresses, the turgor dration persists, oligruria for fullness) ofthe skin is lost. Ifdehy- (reduced urine output) occurs as a compensation for the fluid loss. More severe degrees of fluid loss are accompanied by a shift of water from the in- tracellular space to the extracellular space, a process that causes severe cell dysfunction, panicularly in the brain. Systemic blood pressure falls with continuous dehydration, and declining perfusion eventually leads to death. Fluids in several forms should be continually urged on the patient. In severely dehydrated individuals, they must get to the hospital right away. IV fluids will quickly reverse dehydration, and is often life saving in young children and infants.

Which of the following coagulation factors is deficient in hemophilia B VI VII VIII IX

IX Hemophilia A and B are inherited as a sexJitrked recessiYe trait by which males are allected and females are carriers. The majority ofpeople af{licted with hemophilia have type A and it presents under the age of 25. The signs, symptoms and clinical manifestations include excessive bleeding from minor cuts, epistaxis, hematomas, and hemarthroses. Classifi cations of Hemophilia: . Hemophilia A: considered the classical type, caused by a deficiency of coagulation factor \ lll . (anti-hemophilic factor) Hemophilia B factor) . . produced by hy- (also called Christmas disease): due to a deficiency in fzctor lX (Christmas Hemophilia C (a/s o called Rosenthal's syndrome)', not sex-linked, less severe bleeding. Due to a deficiency qf factor XL Rare disorder but more common in Ashkenazi Jews. lmportant; A true hemophiliac is characterized by having the following: . . . . Prolong€d partial thromboplastin time (PI! Normal protbrombln time (PT) Normal platelet count Normal bleeding time Note: von Willebrand's disease is inherited as an autosomal dominant bleeding disorder, it oc- curs with equal frequency in both seres. Due to the absence ol von Willebrand's factot (VWF), which results in failurc to form a primary platelet plug. Labomtory features include a and prolonged bleeding time. Thrombocytopenia: . Idiopathic thrombocytopenic pupnr^ (ITP)t autoimmune bleeding disorder in which pa- tients develop antibodies against their own platelets. Signs and symptoms: no splenomegaly, su- perficial bleeding ofthe skin, mucous membranes, and genitourinary tract. . Thrombotic thrombocytopenic purpura (TTP)| chaftcterized by severe thrornbocytopenia, micrcangiopathic hemolytic anemia (ftave presence of schislocytes), andneu,rologic abnormalities. Signs and symptoms: fever, neurologic abnormalities, including headache, aphasia, or stupor.

After a stroke on the right side ofthe brain that affects the right upper motor neurons, the tongue deviates to the: Neither ofthe above, the tongue would not be affected Left on protrusion Right on protrusion

Left on protrusion (and the left half of the tongue will atrophy) Lesions of the hypoglossal nerve: . Hypoglossal nerve Iesions paralyze the tongue on one side On protrusion, the tongue deviates to the ipsilateral pending on the lesion site. Lower motor neuron lesion: Lesions to the hypoglossal nerve causes paralysis on the ipsilateral or contralateral side, de- fsame) side: Tongue deviates to the paralyzed side on protrusion (the paralwed muscles v,ill lag. cartsing th? tip to dcviote). . . Musculature atrophies on the paralyzed side Tongue fasciculations occur on the paralyzed side Example: With a neck wound that cuts the right hypoglossal nerve, the tongue deviates to the right on protrusion, and the right half of the tongue will later demon- strate atrophy and fasciculations Upper motor neuron lesion: Causes paralysis on the contralateral side: . . Tongue deviates to the side opposite the lesion Musculature atrophies on side opposite the lesion Example: After a stroke on the right side of the brain that affects the right upper motor neurons, the tongue deviates to the left on protrusion, and the left half of the tongue will atrophy Important: If the genioglossus muscle is paralyzed, the tongue has a tendency to fall back and obstruct the oropharyngeal airway with risk of suffocation.

When a biopsy is being performed it ls important to: Incise perpendicular to the long axis ofany muscle fibers beneath the lesion Incise parallel to the long axis ofany muscle fibers beneath the lesion Incise as deep as possible into muscle fibers beneath the lesion Incise at a 45 degree angle to the long axis ofany muscle fibers beneath the lesion

Incise parallel to the long axis ofany muscle fibers beneath the lesion *** Whenever possible, the incisions should be oriented parallel to lines ofmuscle tension in order to minimize scarring and wound dehiscence. Note: Biopsy incisions on the face should be oriented to follow Langer's lines. Four major types ofbiopsy in and around the oral cavityl . C)-tologyi should be used as an adjunct to, not a substitute for, biopsy. Indications include: $ hen large areas ofmucosal change must be monitored for dysplastic change, such as herpes or pemphigus. Technique: the lesion is scraped repeatedly and firmly with a moistened tongue depressor or cement spatula. The cclls obtained are smeared evenly on a rs inrnediately immersed in a fixing solution and cxamincd under lhe microscope. ..\spiration biopsy or fine needle aspiration /FN,4): fDlI): glass slide, and the slide is the use ofa needle and syringe to pen- errate a lesion lbr aspimtion ofits contents. Indications include: it should be carried out on all lcsions thought to contain fluid (rith the possible exception ofa mucocele) or any intraosseous lc,rion belbre surgical exploration. Technique: an l8-gauge needle is connected to a 5 or l0 ml s1 ringe. The area is anesthetized and the I 8-gauge needle is inserted into the depth of the mass during aspiration. . Incisional biopsy: rcmovcs only a representative portion or portions of a lesion along with a representation ofadjacent normal tissue. Indications: ifthe arca under investigation appears diflicult to excise because ofits extensive size cation, or whenever there is a . (larger than I cm itl diameter) or hazardous lo- great suspicion ofmalignancy. Excisional biopsy: entails removal ofthe entire lesion along with at least 2 mm ofnormal mar- ginal tissuc frorn the sides of the lesion. This technique should bc employed with smaller lesions i/1".rs tlrd, I cu in diameter) that on clinical examination appear to be benign. lmportant: It can not bc ovcremphasized that all pertinent clinical information and the findings of other diagnostic modalities must b€ provided to the pathologist at th€ time ofthe initial submission ofthe specimen.

Which of the following is that phrase of anesthesia that begins with the adminlstration of anesthetic and continuing until the desired level of patient unresposiveness is reached Induction Maintenance Recovery

Induction Stage I and Stage II of general anesth€sia together are referred to as induction. The depth ofgeneral anesthesia fby irhalation) vnies with the partial pressure (tension) of the anesthetic agent in the brain, and lhe rates ofinduction arrd recovery depend upon the rate ofchange oftension in this tissue (also blood supply to the lungs, pulmonary ventila- tion, and the concentration ofthe qnesthetic influence the rate of induction). signs and stages of anesthesia are most likely to be seen with anesthetic that has a slow rate of in- duction. L Maintenance is the process ofkeeping a patient in surgical anestlesta. 2 . Recovery is the phase of anesthesia commencing when surgery is complete and the delivery of the anesthetic is terminated and ending when the alesthetic has been eliminated from the body. 3. The behavior of patients under general anesthesia suggests that the most re- sistant part ofthe CNS is the medulla oblongata (cardiac, vasomotor, and res- piratory centers of the brain). 4. The most controllable route for administration of a general anesthetic is in- halation. 5. Minimum alveolar concentration {MAC): alveolar concentration ofanesthetic at which 50% ofthe palients are unresponsive to a standard surgical stimulus. 6. Meyer-Overton theory: anesthesia commences when a chemical substance reaches a certain molar concentmtion in the hydrophobic phase. 7. Second gas effect: this occurs when one gas speeds the rate ofincrease ofthe alveolarpartial pressure ofa second gas. Potent agents are administered with ni trous oxide so that the potent agent will be delivered in increased amounts to the alveoli as gas rushes to replace the nitrous oxide absorbed by pulmonary blood.

Trauma to muscles or blood vessels in the ? ls the most common etiological factor in trismus associated with dental injections of local anesthetics, Pterygoid fossa Temporal fossa Submandibular fossa Infratemporal fossa

Infratemporal fossa Limited jaw opening, or trismus, is a relatively common complication following local anesthetic administration. In addition to tmuma to muscles or blood vessels in the infratemporal fossa, it may be caused by hematoma formation, localized muscle necrosis secondary to the anesthetic drug or vasoconstrictor, infection in the fascial space, or introduction ofa foreign body. Note; In most instances of trismus the patient rcports pain and some difficulty opening his or her mouth on the day after treatment in which a posterior superior alveolar or inferior alveolar nerve block was administered. The main symptom of trismus is the limitation of movement of thc mandible, which is often associated with pain. Symptoms will arise from one to six days following an injcction. The du- ration of symptoms and their severity are both variable. Note: The medial pterygoid muscle is most often af'fected. Management of trismus: . . . . . Apply hot, moist towels to the site for approximately 20 minutcs every hour Warm saline rinses Use analgesics as required Benzodiazepincs 1e.g., Diazepam) for muscle relaxation ifdeemed necessary The patient should gradually open and close mouth as a means ofphysiotherapy Follol ing an inferior alveolar nerve block injection or a mental block injection, a prickly or tingling sensation (paresthesiq), ever' complete numbness in the lower lip, may result and persist tbr a considerable time. This is usually considered to be due to direct trauma or piercing of dre ncrve trunk by the needle. This happens more often in thc case of the mental block in- jection. The symptoms of paresthesia gradually diminish months). a\d recov ery is usually complete. (uoy last from Remember: The most common cause of paresthesia of the lower lip is thc rcmoval of a mandibular third molar (especially horizo lally impqcred ones).

What two areas are impacted maxillary third molars occasionally displaced into? Canine space Pterygomaxillary space Infratemporal space Pharyngeal space . Maxillary sinus

Infratemporal space Maxillary sinus Impacted maxillary third molars are occasionally displaced into two areas: . \Iariflary sinus proach .Infratemporal (antrun): from which they are removed via a Caldwell-Luc ap- space: during elevation ofthe tooth the elevator may force the tooth posteriorly through the periosteur into the infratemporal fossa. If access and light are good, the tooth may be retrieved with a hemostat. lfthe tooth is not retrieved after a shon amount of time, the area should be closed. The patient should be infomed that the tooth has been displaced and will be removed by an oral surg€on who will use a special technique to remove it. \ote: To minimize the chance of dislodging an impacted maxillary third molar into the infratemporal fossa during its surgical removal, develop a full-thickness mucoperiosteal t1ap. bringing the incision anterior to the second molar (add a releasing incision €t\d]'r'l. to improve visualization ofthe impacted tooth and place a broad retractor distal to the molar while elevating it. Remember: L When performing a surgical removal ofa mandibular molar, do not section through the entire tooth. The lingual plate is often thin, and complete sectioning may perforate the plate and injure the lingual nerve. 2. The inferior alveolar nerve most often lies truccal and slightly apical to the roots ofa mandibular third molar. 3. Buccal to lingual movement is not elficient when removing mandibular post€rior teeth because mandibular bone is too dense and does not expand in a similar fashion to that ofthe maxillary bone.

All of the following may prevent a patient from having vasovageal syncopal reaction after the use of local anesthetic except one Slowly injecting the anesthetic solution Watching the patient's color change during the injection Using a topical anesthetic prior to administration ofthe local anesthetic Injecting the anesthetic solution as quickly as possible Using a low concentration of vasoconstrictor Premedicating extremely anxious patients Sympathetic, but confident handling ofthe patient

Injecting the anesthetic solution as quickly as possible The most common cause ofa transient loss ofconsciousness in the dental office is vasovagal syncope. This generally is due to a series ofcardiovascular events triggered by the emotional shess btought on by the anticipation of or delivery ofdental care. Prevention ofvasovagal syncopal reactions involves proper palent preparalon. Remember: Any signs ofan impending syncopal episode should be quickly treated by placing the pa- tient in a supine position with the feet elevated (Trendelenbutg posiliol,/, monitoring vital signs, loos- ening tight clothing and pJacing a cold compress on the forehead. Oxygen 3-4 L/minute should also be given via nasal cannula. Important: The most common early sign ofsyncope is pallor. Vasovagal Syncope: . . . Most common related to injections in younger individuals Parasympathctic response often followed by sympathetic response secondary to anxiety Warm feeling, pale, diaphoresis, "feeling faint or sick," nausea, bradycardia, and hypotension Most Common Medical Emergenciesi . S).'ncope . Asthma attack .Hyperventilation'Acutemyocardialinfatction . . . Hypoglycemia . Seizure Postural hypotension 'Allergic ,{ngina pcctons Postural Hypotension: Management . . . . reactions Slo\\'to change position from laying to sifting to standing \eed for change in medication'l Rcccnt change in medication Rule out precipitating causes "Hl . . . (depends on severity) pervenlilation syndrome"- most commonly seen in dental office Related to anxiety/ panic Associated with lightheadedness. dizziness, chest pain, dysphagia, nausea (CHF), endocnne ( Rule out morc se ous potential conditions including pulmonary (aslhtna, PE), cardia. d i a b et i c ke to ac ido s is)

Codeine, a widely used analgesic in dentistry: Is a natual constituent of opium May be given only by injection Has a calming effect on gastric mucosa Is stronger than morphine, more addictive, and more constipating

Is a natual constituent of opium \crr to morphinc, codcine is thc most important alkaloid of opium. Codeine has two primary thera- ft'rnic c'l1'ecIsr analgesic and antitussivc. Codcine is relatively less polent than morphine and does not have ::e abuse potential ofmorphine. It is more likely than other opioids. othcr than morphine, to cause con- ii:F,r!ion and nausea- Codeine is usually combined with other drugs, for example, Empirin (Aspirin + arrr.rrr./. and Tt-lenol#2,3, and 4 (Acetattinophen + Codeine). \ote: Jlorphine is effectivc in providing reliefofmoderate to severe pain but is associated with the ad- r:rre etTects ofconstipation, nausea, and vomiting. Opr(.id analgesics are thought to inhibit painful stimuli in the substantia gelatinosa of the spinal cord, b::i:r tem. reticular actiYating system, thalamus, and limbic systcm. Opiate receptors in each ofthcse ::eas lnreract \\'ith neuroffansmitters ofthe autonomic nervous system, producing alterations in reaction :.. p.rrnlul stimuli. Actions ofopioid analgesics can be defined by their activity al three specific recepior i' p3i: . . . \lu receptors: - \Iul: analgesia - Mu2: respiratory depression. bradycardia, physical dcpcndence, euphoria Xappa receplors: analgesia, sedation, dysphoria, psychomimetic effects Delta r€ceptors: analgcsia. moduiates activity at the mu recepto.

Dissociative anesthesia is a unique method of pain control that reduces anxiety and produces a trancelike state in which the person is not asleep, but rather feels separated from his or her body. The primary medication used is: Demerol Ketamine Pentobarbital Promethazine hydrochloride

Ketamine Dissociative anesthesia is useful in emergency situations, such as an injury. It can also be used for short procedures that are painful, such as changing bandages. This method is safe and lasts only a short time. Because a person does not usually recall the procedure, this method is useful in children. The primary medication used is called ketamine. A sedative is often given before ketamine to reduce anxiety. Note: A person who has had dissociative anesthesia usually does not remember the procedure, especially if a sedative has been given along with the pain medication. Most people feel back to normal within a few hours. As the medication wears off, an individ- t;.aI (particularly adult patients) may have intense dreams and even hallucinations. Ketamine, a phencyclidrLne (PCP) deivative, is l0 times more lipid soluble than thiopental, enabling it to cross the blood-brain barrier quickly. It produces dissociative anesthesia. which can be seen on EEG as dissociation between the thalamus and limbic system. Rapid CNS depression with hypnosis, sedation, amlesia, and intense analgesia occurs in 30-60 seconds after administration. The anesthetic induction doses are l-2 mg,&g IV, with effects lasting 5-10 minutes or 10 mg/kg intramuscular, which acts in 2-4 minutes. Ketamine: . . . . . Increases airway secretions, creating the need for anticholinergics such as glycopyrr- olare in the preoperative period lncreases BB heart rate, and cardiac output , but not respirations Produces bronchial smooth muscle relaxation because of sympathetic stimulation [s a potent cerebral vasodilator Side effects include: hypertension, increased pulse and delirium

The initial cllnical signs and symptoms of CNS toxicity for local anesthetics are usually excitrtory in nature. However, it is also possible that the excitatory phase of the reaction may be extremely brief or may not occur at all. This is true especially with which two Iocal aneshetics? Lidocaine Tetracaine Etidocaine Procaine Bupivacaine

Lidocaine, Procaine Local ancsthetics readily cross the blood-brain barrier Their phannacological action on the CNS is depression, At low (therapetic, nontoxic) bloodlevels, there are no CNS eflects ofany clini- cal significance. At higher (toxic, overdose) levels,thc primary clinical manifestation is a generalized tonic-clonic convulsion. With a furthcr incrcase in the blood level ofthe local anesthetic above its "therapeutic" level, adverse reactions may be observed. Because the CNS is nuch morc susceptible to the aclions oflocal anesthetics than other systems, it is not surprising that thc initial clinical signs and symptoms of overdose (toicity) are CNS in origin. Initial clinical signs and symptoms (slurred speech, tlizziness, talkctiveness, apprehension, incrcased anxiety) ofCNS toxicity are usually excitatory in nature. Lidocaine and procaine differ somcwhat from other local anesthetics in that lhe usual progression of signs and syn'tptoms may not be seen. Lidocaine and procaine frequently produce an initial mifd sedation or drovsi\ess (here common with lidocaine). Sedation may develop in place of the excitatory signs. Ifeither excitation or sedation is observed in the initial 5 to l0 minutes alicr thc intraoral administration ofa local anesthetic, it should serve as a wamirg to the clinician ofa rising local anesthetic blood level and the possibility (if level co li ues to risel ofa more serious reaction, possibly a gcncralized conl'ulsive episode. Local anesthetics havc a direct action on the myocardium and peripheral vasculature ln general, ho$ever, thc cardiovascular system appears to be nore resistant to the effects oflocal anesthetic drugs than the CNS. . Direct action on the myocardium: Local anesthetics produce a myocardial dcpression that is related to the local anesthetic blood level. Local anesthctics decrease electrical excitability ofthe myocardium, decrease the conduction rate, and decrease the lbrce ofcontraction . Direct action on the peripheral vasculature: All local aneslhetlcs (except cocaine and ropi- tacaine) produce a peripheral vasodilation, through relaxation of the smooth muscle in the walls ofblood vessels.

The ? rises from the anterior surface of the external carotid artery opposite the tip of the greater cornu of the hyoid bone Submental artery Inferior alveolar artery Lingual artery Ascending pharyngeal artery

Lingual artery ft loops upward and then passes deep to the posterior border ofthe hyoglossus muscle to enter the submandibular region. The loop ofthe artery is crossed superficially by the hy- poglossal nene. The lingual artery supplies structures ofthe floor ofthe mouth and the posterior and inferior surface ofthe tongue. Major branches include the : . . . Suprahyoid artery: supplies the suprahyoid muscles Doral lingual artery: supplies the tongue, tonsils, and soft palate Sublingual artery: supplies the floor ofthe mouth, mylohyoid muscle, and sublin- gual gland . Deep lingual artery: supplies the tongue Important: The lingual artery does not accompany the conesponding nerve throughout its course. Remember: The inferior alveolar nerve, artery, and vein along with the lingual nerve are found in the pterygomandibular space between the medial pterygoid muscle and the ramus ofthe mandible. The inferior alveolar nerve passes lateral to the sphenomandibu- lar ligament. The submandibular duct is crossed twice by the lingual nerve. Ifthe lingual nerve is cut after the chorda tympanijoins, there will be loss ofboth taste and tactile sen- sation. Note: The lateral pterygoid muscle forms the roofofthe pterygomandibular space.

The primary site of biotransformation of amide drugs is the Plasma Kidney Liver Lung

Liver A significant difference between the two major groups of local anesthetics, the esters and the amides, is the means by which the body biologically transfoms the active drug into one that is phar- macologically inactive. Metabolism (or biotransformationl of local anesthetics is important bc- cause the overall toxicity of a drug depends on a balance between its rate of absorption into the bloodstrcam at the sitc ofinjection and its mte ofremoval from the blood through the processes of tissue uptake and metabolism. The primary site of biotansformation of amide drugs is the liver. Ester local anesthetics are hy- drolyzed in the pfasma to pala aminobenzoic acid (PABA) by the enzyne pseudocholinesterase. Pa- tients with pseudocholinesterase inactivity are unable to detoxily ester tlpe agents at a normal rate. Amide type anesthetics are recommended in these patients. Allergic reactions to amide type local anesthetics are rare but may occur as a result ofhypersensi- tivity to thc local ancsthetic agent itselfor due to an allergy to methylparaben or other preserva- tives used in many solutions. These reactions are characterized by cutancous lesions of delaycd onset or urticaria, edema, and other manifestations ofallergy. Important: For thosc patients allergic to both cstcr and amide type local anesthetics, Diphenhydramine is a safe and effective alternalive.

All of the following drugs can reduce salivary flow during dental procedures. Which one works by reducing anxiety and sensitivity during the procedure Scopolamine Atropine Local anesthesia Benztropine

Local anesthesia Local anesthesia acts by reducing sensitivity which therefore reduces anxiety and stress re- lated to treatment; salivation is also decreased. Scopolamine, atropine and benztropine are anticholinergic drugs. Not only do they decrease the flow ofsaliva, but also decrease the secretion fiom respirctory glands during general anes- thesia. l. The duration of action of local anesthetics is directly proportional to protein binding and lipid solubility. Increased protein binding biliry - increased duration ofaclion. -increased 2. The lower the pKa (dissociation constant) of the local anesthetic, the faster the onset ofaction. Important point: a local anesthetic with a low pKa has a very large number oflipophilic free base molecules that are able to diffuse through tbe nerve membrane. 3. Increased blood flow -shorter duration of action. 4. Metabisulfite is an antioxidant that protects the vasoconstrictor from oxidation. It has a low incidence of allergenicity. 5. The local aresthetic prilocaine can produce methemoglobinemia in patients with subclinical methemoglobinemia when administered in large doses. The topical anesthetic benzocaine also can induce methemoglobinemia, but only when administered in very large doses. 6. The administration of norepinephrine and levonordefrin should be avoid€d in patients receiving tricyclic antidepressants. There is an increased sensitivity to vasoconstrictors. *** Epinephdne should be used cautiously. 7. The administration ofvsoconstrictors in patients being ffeated with nonselective beta-blockers (i.e., Propranolol) increases the likelihood ofa serious elevation ofthe blood pressure accompanied by a reflex bradycardia. Use vasoconstricton cautiously.

Which is the least lipid soluble of the three main benzodiazepines resulting in a slow onset of action but a long duration of action Midazolam Lorazepam Diazepam

Lorazepam Anterogmde amnesia, minimal depression of ventilation and the cardiovascular system, and sedative properties make benzodiazepines favorable preoperative medications. Clinical uses for benzodiazepines include: preoperative medication, IV sedation, induction of anesthesia, maintenance ofanesthesia and suppression of seizure activity. Benzodiazepines act by poten- tiating the action of GABA, an amino acid and inhibitory neurotransmitter, which results in increased neuronal inhibition and CNS depression. Benzodiazepines bind to specihc benzodiazepine receptor sites, which are found on postsynaptic nerve endings in the CNS. Benzo- diazepines are the most effective oral sedative drugs used in dentistry. The most common benzodiazepines used as amnestics in anesthesiology are: midazolam (most co m mon). lorazepam. and diazepam. . iN{.id^zolam (Uersedl: is the most lipid soluble ofthe three and, as a result, has a rapid onset and a relatively short dumtion ol action. Is prepared as a water-soluble compound that is transformed into a lipid-soluble compound by exposure to the pH ofblood upon injection. This unique property ofmidazolam improves patient comfort when administered by the IV or lM route. This prevents the need for an organic solvent such as propylene glycol, which is required for diazepam and lorazepam. . Diazeparn (Velium): is water-insoluble and requires the organic solvent propylene glycol to dissolved it. The onset time is slightly slower than that of midazolam. . Lorazepam (Ativan)r ls the least lipid soluble ofthe three main benzodiazepines, resulting in a slow onset ofaction but long duration ofaction. It requires propylene glycol to dis- solYe it. which increases its venoirritation. Lorazepam is a more powerful amnestic agent than midazolam, but its slow onset and long duration ofaction limit its usefulness for pre- operative anesthesia. 1. Chloral hydrate is a sedative and hlpnotic that is widely used for pediatric se- dation. 2. Emotional stress decreases the rate ofabsorption ofa drug when given orally.

Which of the following exits the skull through the foramen ovale Ophthalmic nerve Maxillary nerve Facial nerve Mandibular nerve

Mandibular nerve Ihe ophthalmic nerve (Vl) enters the middle cranial fossa through the superior orbital fissure and courses within the lateral wall ofthe cavemous sinus on its way to the trigeminal ganglion. The maxil- lart nerve 4r) enters the middle cranial fossa through foramen rotundum and may or may not pass !hroueh thc cavemous sinus en route to thc trigeminal ganglion. The mandibular nerve middle cranial fossa through foramen ovale, coursing directly into the ttigcminal ganglion. The trigcm- inal ganglion 1n. if. a. r enilttnar ganglion ) lies in a depression known as the trigeminal cave car er. Thc trigeminal nervc cxits the trigeminal ganglion and cou$cs "backward" to entcr thc mid-lat- eral aspect ofthe pons. The mandibular division is the largcst ofthc 3 divisions ofthe trigeminal nerve. It has motor and sen- so+ functions. It is created by a large sensory alld a small motor root that unitsjust after passing through rhe foramen ovale to enter the iniiatemporal fossa. It immediately gives rise to a meningeal branch and Ihen di!idcs into anterior and posterior divisions. -\nterior Division: Smaller, mainly motor, with I sensory branch . . . (huccal): \lasseteric: innenates thc masseter muscle and provides a small branch to the TMJ Anterior and posterior deep temporal: innervates the temporalis muscle )Iedial pter!goid: innervates the medialpterygoid muscle . Lateral pterygoid: innervatcs the lateral pterygoid muscle . Buccal: supplies the skin ovcr the buccinator muscle before passing through it to supply the mucous membrane lining its inner surface and the gingiva along the mandibrlar molars Posterior Division: Larger, mainly sensory with I motor branch frene to m!-lohroid)l . . Auriculotemporali supplies the TMJ, auricle, and extemal auditory meatus Lingual: supplies the mucous membrane ofthc anterior 2/3 ofthe tongue and gingiva on the lin- gual side ofthe mandibular teeth . lnferior alveolar: largest branch ofthc mandibular division; innervates all mandibular teeth and the gingiva from the premolars anteriorly to the midline via the mental branch . Mylohyoid: supplics thc mylohyoid and the anterior belly ofthe digastric muscle Remember: The trigeminal ncrve contains no parasympathetic component at its o.igin.

The most commonly impacted teeth are the mandibular third molars, maxillary third molars, and the: . Maxillary lateral incisors Mandibular first molars Mandibular premolars Maxillary canines

Maxillary canines Classifications of impacted teeth Angulation: Mesioangular (most dillicult to remove fol lecsl diJlicult to rcmove for mandibular impaclionsl, distoangular mandibulu impactions),v ertical and horizontal Pell and Gregory Classification: rclationship to anterior border ofthe ramus . . . Class 1: normal position anterior to the ramus Class 2: one-halfofthe crown is within th€ ramus Class 3: entire crown is embedded within the ramus Relationship to occlusal plane: . . Class A: tooth at the same plane as othgr molant Class B: occlusal pane ofthird nolar is between the occlusal plane and the cervical line of the second molar . Class C; entire crown is embedded within the mmus

The optimum site for IV sedation for an outpatient is the Median basilic vein Median cephalic vein Median antebrachial vein Axillary vein

Median cephalic vein This Vein lies in the lateral aspect ofthe antecubital fossa (anterior to the elbow). Avord entering the brachial artery. If the artery is entered, the following symptoms will ap- pear: irnmediate buming at the site ofthe injection, the arm will appear blotchy, and the pulse in the arm v ill be weak compared to the other arm. IV Sedation: . . . Usually done with a 21 gauge needle Popular drug is Valium (Diazepam) The rate of injection of Valium is a I nrr mrnure - 1 ml of injectable Valium contains 5 mg of Valium . Injection is discontinued when the eyelids droop (ptosis) Three common signs indicating when the correct level of sedation has been reached when usins Vaf ium: 1. Blurring ofvision 2. Slurring ofspeech 3. 507o ptosis ofthe eyelids (this is called Ver- rill's sign) Remember: Valium is contraindicated for use in a patient with a history of narrow angle glaucoma.

? should be used cautiously in the elderly. lt should never be given to patients on mono|mine oxidase inhibitors for psychiatric disease and is generally contraindicated in patients receiving phenytoin (Dilantin) for seizure disorders. Acetaminophen Meperidine Codeine Ibuprofen

Meperidine Meperidine (Demero, is a synthetic opioid analgesic with less potency than morphine. It is used for the reliefofmoderate to severe pain, for preoperative sedation, for posloperative anal- gesia, for obstetric anesthesia, and when given IV for supportive anesthesia. lt is probably the most widely used narcotic in Americzm hospitals. It should be used with particular caution, if at a)l, in the elderly. lt is the drug ofchoice among drug abusers and must be used with extreme caution. Meperidine is the most abused drug by health professionals. The onset ofaction is more rapid, but the duration ofaction is shorter, than that ofmorphine. Note: It produces slight euphoria but no miosis. \.leperidine is often prescribed as 50 mg every 4 hours as needed for pain. It is often simulta- neously presribed with the drug promethazine (Phenergan) in 25-50 mg doses every 4 hours. The promethazine is a sedative and eniances the effect ofmeperidine. Therefore, less meperi dine r-ields more analgesia when in combination with promethazine. In addition, promethazine is an anti-emetic, which helps negate some ofthe side effects ofmeperidine, namely, nausea. Important: Concomitant administration ofmeperidine and MAO inhibitors has resulted in life-threatening hyperpyrexic reactions that may culminate in seizures or coma. Monoamine oxidase (MAO) inhibitors are a class ofdrugs used for depression and Parkinson's Disease. Ex- amples of MAO inhibitors include isocarboxazid (brand name Marplan), phenelzine (Nardil), rranylcypromine /Parnate), ard selegiline (E ldepryl). \lechanism of action: thought to act by increasing endogenous concentrations of norepi- nephrine, dopamine, and serotonin through inhibition ofthe enzyme (monoamine oxidase) re' sponsible for the breakdown of these neurolmnsmillers. r-ote: There is a decreased effectiveness ofmeperidine in the presence of phe\ytoir (Dilan' tin) R€memb€r: Morphine is the standard drug to which all analgesic drugs are compared. lt causes €uphoria, analgesia, and drowsiness along with miosis and respiratory depression.

Which of the following acid base abnormalities will occur in a patient with recurring vomiting of gastric contents Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

Metabolic alkalosis Acid-Base Disorders: . Normal range: pH = Acidosis vs Alkalosis . . '7.35 - 7.45 Bicarbonate = 22-26 mtrol/L IfpH is less than 7.35, the patient is acidemic lfpH is greater than 7.45, the patient is alkalemic Determine primary process . After evaluating pH, look at PCO2 and bicarbonate - IfpH is acidemic and PCO2 is greater than 45 mmHg, the primary procoss is respiratory; if bicarbonate is less than 22, the primary process is metabolic - IfpH is alkalemic and the PCO2 is less than 35 mmHg, the primary process is respiratory; ifbicarbonate is greater than 26, the primary process is metabolic. Metabolic acidosis: Etiologies- diabetic or starvation ketoacidosis, lactic acidosis, uremia, severe dehydration. Clinical manifestations: Dyspnea on exertion and nausea and vomiting are common Metabolic alkalosis: Etiologies- vomiting, diuretic use, Cushing's syndrome, Conn sl,ndrome, and exogenous steroids Clinical manifestations: CNS symptoms such as confusion, delirium, and coma. Cardiac ar- rhythmias and hypotension may be noted Respiratory acidosis: Etiologies- COPD, asthma, severe pneumonia or pulmonary edema, CNS depression fdrag.s, CNS event), acute airway obstmction, pneunothorax Clinical manifestations: Related to degree and duration ofacidosis and presence ofhypoxia. In acute disease, CNS symptoms such as confusion, anxicty, psychosis, and seizures may be noted: In chronic disease, there is lethargy, fatigue, and confusion Respiratory alkalosis: Etiologies- anxiety, hypoxia, CNS discase, drug use (salicylates), pregnancy, sepsis Clinical manifestations: May cause dizziness, perioral paresthesias, confusion, hypotcnsion, stezures. and coma

The maxillary first molar is innervated by Anterior superior alveolar and middle superior alveolar nerves . Middle superior alveolar and posterior superior alveolar newes . Posterior superior alveolar and inferior alveolar nerves . Middle superior alveolar nerves and palatine nerves

Middle superior alveolar and posterior superior alveolar newes . The posterior superior alveohr fP,Sl) nerve block, otherwise known as the tuberos- ity block or the zygomatic block, is used to achieve anesthesia for the pulps ofth€ max- illary third, second, and first molars (entire tooth = 7226; mesiobuccal root of the marillary first molar not anesthetized: 28%o). Target area: PSA nerve superior, and medial to the posterior border of the maxilla. Note: Potential for hematoma formation. . The middfe superior veolar (MSA) nerve block is useful for procedures where the maxillary premolar teeth or the mesiobuccal root ofthe first molar require anesthesia. Target area: maxillary bone above the apex ofthe maxillary second premolar. Note: The MSA nerve is present in only about 28% ofthe population. . The anterior superior alveolar (ASA) nerve block or infraorbital nerve block provides profound pulpal and buccal soft-tissue anesthesia from the maxillary central incisor through the premolars in about 72 of patients. Target area: infraorbital foramen (belov' the infraorbital notch). o/o Remember: In order to extract the maxillary first molar, you must numb both the PSA and MSA nerves as well as the greater (anterior) palatine newe for palatal anesthesia lsolt tissuel.

The sublingual gland is locatsd in the oral cavity betwe€n the mucosa of the oral cavitv and the: Masseter muscle Mylohyoid muscle Buccinator muscle Temporalis muscle

Mylohyoid muscle The sublingual glands are located in the floor ofthe mouth beneath the tongue, close to the midline. It lies between the sublingual fossa of the mandible and the genioglossus muscle ofthe tongue. The mylohyoid muscle supports the individual sublingual glands in- feriorly. Unlike the submandibular gland, which drains via one large duct, the sublingual gland drains via approximately l2-20 small ducts fRivian's ducts),the majority open into the mouth on the sumrnit ofthe sublingual fold, but a few open into the submandibular duct. The sublingual gland is ifflervated by parasympathetic secretomotor fibers from the facial nerve, which run in the chorda t)rynpani and in the lingual nerve (branch of V-3) and synapse in the submandibular ganglion. The blood supply comes from branches ofthe facial and lingual arteries. The veins drain into the facial and lingual veins. The lymph ves- sels drain into the submandibular and deep cervical lymph nodes. Important: . The lymph vessels ffom both the sublingual and submandibular glands drain into the submandibular and the deep cervical lymph nodes . Bartolin's duct, a common duct that drains the anterior part ofthe sublingual gland in the region ofthe sublingual papilla, may be present . . The submandibular duct lies on the sublingual gland The sublingual gland is a mixed salivary gland, secreting both mucous and serous saliva, but predominantly mucous-secreting \ote: Von Ebner's glands are located around the circumvallate papilla ofthe tongue. Their main function is to rinse the food away from the papilla after it has been tasted by the taste buds. They are purely serous.

Which nerve may in some cases also serve as an afferent nerve for the mandibular first molar which needs to be considered when there is failure of the inferior alveolar local anesthetic block Posterior superior alveolar nerve Glossopharyngeal nerve Facial nerve Mylohyoid nerve

Mylohyoid nerve After the inferior alveolar nerve exits the mandibular canal, a small branch occurs, called the mylohyoid nerve. This newe pierces the sphenomandibular ligarnent and runs inferiorly and anteriorly in the mylohyoid groove and then onto the inferior surface ofthe my- lohyoid muscle. The mylohyoid nerve serves as an effetent nerve to the mylohyoid muscle and the anterior belly ofthe digastric muscle. This nerve may in some cases also serve as an afferent nerve for the mandibular first molar. The mylohyoid muscle is an anterior suprahyoid muscle that is deep to the digastric mus- cle. In addition to either elevating the hyoid bone or depressing the mandible, the muscle also forms the floor ofthe mouth and helps elevate the tongue. Note: The sublingual gland is located superior to the mylohyoid muscle. . . l. When placing the film for a periapical view of the mandibular molars, it is Note{r the mylohyoid muscle that gets in the way if it is not relaxed. ':;t;;i 2- when the floor ofthe mouth is lowered surgically, the mylohyoid and g€nioglossus muscles are detached. 3. An injection into the parotid gland (capsule) uthen atlempting to administer an inferior nerve block may cause a Bell's palsy facial expression ofthe forehead muscles, the eyelid and ofthe upper and lower lips on the same side ofthe face that the injection was given. Important: Ifthe parotid capsule injection happens, care must be taken to protect the eye from injury and drying using lubrication and an eye patch. 4. Remember: The bone of the maxilla is more porous than that of the mandible, therefore, it can be infiltrated anywhere.

Which of the following will produce neurolept anesthesia Neuroleptic agent + narcotic analgesic . Neuroleptic agent - nitrous oxide Neuroleptic agent + narcotic analgesic + nitrous oxide Narcotic analgesic + nitrous oxide

Neuroleptic agent + narcotic analgesic + nitrous oxide Neurolept anesthesia is a state of neurolept analgesia and unconsciousness, produced by the combined administration ofa narcotic analgesic and a neuroleptic agent, together with the inhalation ofnitrous oxide and oxygen. Neurolept analgesia only produces an unconscious state ifnitrous oxide is also adrninistered below). Neuroleptic agent + narcotic analgesic = neurolept analgesia (Droperidol) (l'entanyl) (conscious) Under the influence ofthis cornbination, the patient is sedated and demonstrates psychic indiffer- ence to the environment yet remains conscious and can respond to questions and commands. Neurolcpt + nitrous oxide = neurolept anesthesia analgesia in oxygcn (wtconscious) Induction of anesthesia is slow, but consciousness retums quickly after the inhalation ofnitrous oxide is stopped. 1. Neurolept analgesia is useful for minor surgical procedures, somc radiological pro- Note3i. cedues, bum dressing, and endoscopy. ,.r.._,,.i 2. Neuroleptic agents such as droperidol (laapsine) causc areduction in all-{iety and a state of indift'erence. 3. Droperidol is an antiemetic and has adrenergic blocking (a/p ha block) activity. 4. Neurolept analgesia,/anesthesia may be especially useful in the elderly, debilitated or seriously ill patient. 5. The combination ofdroperidol and fentanyl (Sublimaze),is lnnovar. 6. Innovar produces slight circulatory effects, but can cause siSnificant respirutory depression. 7. The low incidence of extmpyramidal side effects associated with droperidol use may bc cffectively treated with the anti-cholinergic (anti-muscairlc, dmg, benztropine (Coge tin).

How will a larger than norm|l functional residual capacity affect nitrous oxide sedation? Nitrous oxide sedation will happen much quicker Nitrous oxide sedation will take longer Functional residual capacity does not affect nitrous oxide sedation

Nitrous oxide sedation will take longer The functional residual capacity is the amount ofair remaining in the lungs at the end of the normal expiration. Note: This air is used to provide air to the alveoli, which will aerate the blood evenly between breaths. Note: Pulmonary volumes and capacity are about 20 to 25o% less in females than in males and are greater in large and athletic persons. Nitrous oxide sedation will vary accord- ingly. R€spiratory air volumes during rest and exercise are of physical and clinical interest and they can be measured using a spirometer. The main volumes ofinterest are: . Tidal Volume (TV): amount of air breathed in and out during quiet breathing . Expiratory Reserve Volume (ERV): amount ofair forced out ofthe lungs in a maximal expiration, over and above that expired in normal breathing . Inspiratory Reserve Volume (IRV): amount ofair inlaled in a maximal inspiration, over and above that inhaled in normal breathing . . \'ital Capacity (VC): TV + ERV + IRV Residual Volume (RV): volume of air that remains in the lungs at all times (can't be neosured by spir)metry) . Total Lung Capacity (TLC): VC + RV

A sedative dose of a barbiturate should be expected to produce Respiratory depression . Minor analgesia . Decreased BMR . All ofthe above effects . None ofthe above effects

None ofthe above effects Properties of barbiturates: . . . CNS depressants: CNS depression with barbiturates is additive with alcohol and opioids Have no significant analgesic effect even at doses that produce general anesthesia Ha\e anticonvulsant effects \Iechanism of action of barbiturates: . Barbiturates inhibit depolarization ofneurons by binding to the GABA recepton, which enhances the transmission ofchloride ions. Barbiturates: . . \\'ell absorbed orally, distributed widely throughout the body \lerabolized in the liver to inactive metabolites that are excreted in the uflne Therapeutic uses of barbiturates: . -{nesthesia: inlluenced by duration ofaction. Thiopental is an ultra-short acting barbitu- rute used IV to induce surgical anesthesia. Note: After IV administration, the last tissue to become saturated as a result of redistribution is fat (as conrpared to liver, brain, and mus- . ,{nticonvulsant phenobarbital used in long-term management of tonic-clonic seizures, status epilepticus and eclampsia . Anxiety: can be used as mild sedatives to relieve anxiety and insomnia Drug interactions: CNS depressants, alcohol, and opioid analgesics enhance the CNS de- pression of barbiturates. Important: Barbiturates can lead to excessive sedation and cause anesthesia, coma and even death. Barbiturate overdoses may occur because the effective dose of the drug is not too far away ftom the lethal dose. Note: The barbiturates can produce fetal damage when administered to a pregnant woman.

Lrrlngospasm is an uncontrolled/involuntary muscular contraction ofthe laryngeal cords. It is a well known, infrequent but serious post-surglcal complication. In the operating room it is treated by administering: Nitrous oxide Oxygen Epinephrine Enflurane

Oxygen A patient under general anesthesia loses the laryngeal reflex. Ifblood and saliva collect (aryngospasm) and the vocal cords will close. When this happens, air cannot pass through and hence the prob- near the vocal cords, this stimulates the patient to go into spasrn lem. The two most important steps in the initial management of a laryngospasm are ap- pl-"-'ing oxygen under positive pressure and administering succinylcholine. \ote: Succinylcholine is a skeletal muscle relaxant that is used when performing endotracheal intubation and endoscopy procedures. Laryngospasm is frequently cited as an adverse effect of ketamine, but it is rarely ob- sened. Frequently, deep, heavy, loud respirations mistaken for laryngospasm are actu- ally due to airway positioning. Such breathing is managed simply by repositioning the patient's head. True laryngospasm during ketamine sedation is usually caused by stimu- lation ofthe vocal cords by instrumentation or secretions.

Following a local anesthetic injection anethetic effects will disappear and reappear in a definite order. Arrange the following in increasing order of resistance to conductance Touch Warm Deep pressure Pain Cold Motor

Pain, cold, warm, touch, deep pressure, motor Local ancsthesia causes loss of sensation by first blocking nerve conduction in thc smaller un- myelinated fibers that carry pain, and then progressing to the larger myelinated llbers for pressure and motor function. This phenomenon is called differential blockade. Differential blockade may be due to the size ofthe nerve, the p.esence or absence ofmyelin, and firing frequency. . Size of nerve: local anesthetics prefcrentially block small fibers bccausc the distancc ovcr which such fibers can passively propagate an electrical impulse is shorter During the onset of local anesthesia, when short sections ofnerve are blocked, the small diameter fibers are the first to fail to conduct. . Preserce or absence of myelin: For myelinated nerves, three successive nodes of Ranvier must by blocked to halt impulse propagation. The thicker the nerve fiber, the farther apart the nodes tend to be, which explains, in part, the greate. resistance to block of lary€ fibers (e.g., nlotorfbers to skeletol muscle). Myelinated fibers tend to become blocked before unmyelinated fibers of the same diameter n-ote: Sodium channels are very dense at the nodes of Ranvier in nvelinated fibers which contributes to thern being blocked before unmyelinated libers of the same drameter. . Firing frequency; sensory fibers, especially pain fibers, have a high firing rate and a rela- ti\ cly long action potential duration to 5 msec). Motor fibcrs fire at a slower rate and have shoner action potential duration (< 0.5 msec).AdeltaandC fibers are small diameter fibers that frp participate in high-frequency pain tnnsmission. Therefore, they are blocked sooner with lower concentmtions of local anesthetics than are A alpba (motot) frbers to skeletal muscle. \otel Nerves regain function in reverse order. The e\tent ofanesthesia depends on a variety offactors, including the amount ofmedication used, bodl temperature, pH, the arnount of protein binding, and dilution by tissue fluids. Local ancs- rhctics work by blocking the flow ofsodium ions, thereby preventing depolarization ofthc nerve tlber and conduction or transmission ofthe imDulse.

Which of the following is the primary direction of luxation for extracting maxillary deciduous molars Buccal Palatal Mesial Distal

Palatal As opposed to the buccal direction in adults. This is because the deciduous molars are more palatally positioned and the palatal root is strong and less prone to fracture. In general. the removal of deciduous teeth is not difficult. It is facilitated by the elastic- it1. of young bone and the resorption of the root structure. Do not use the forceps for extraction of lower primary molars because the sharp beaks ofthese forceps could cause damage to the unerupted pennanent premolar teeth. l. If the preoperative radiograph shorvs that the permanent premolar is \ot€ wedged tightly between the bell-shaped roots ofthe primary tooth, the best treatment is to section the crown of the primary molar and remove the two portions separately. This will help in not disturbing the permanent tooth. 2. After extraction ofmandibular teeth on a child in which mandibular block was given, always advise child not to bite on his/her lip while he or she is numb. lnform Darents as well to watch the child so this does not occur.

The propylene glycol in IV valium can cause Cellulitis . A unilateral facial paralysis Phlebitis Syncope

Phlebitis Phlebitis is irritation or inflammation ofa vein. it is sometimes seen after IV administration ofval- ium. This is usually attributed to the presence ofpropylene glycol in the mixture. Phlebitis is more likely to occur if a vein in the hand or wrist is used and may be more common following repeated injections, especially in heary smokers, the elderly. and women taking oral contraccptivcs. Common signs and symptoms ofphlebitis: . . . Pain Tendcmess Edema . . Erythema Streaking ofthe limb Treatment: Remove the IV catheter, elevate the affected linb, apply warm, n.roist packs to thc in- I gm IV bolus push etety I hours), for appropriate staphylococcus coveragc. fected site, initiate IV ant:biot:Lcs (pre./brably celazolin [Ancefl, Thrombosis is the formation of a blood clot that may partially or completely block a blood ves- sel. A clot located in an inflamed, blood vessel is called thrombophlebitis. Virchow's triad is the name given to the thrce chicfcauscs ofdeep venous thrombosis ( l) damage to the endothelial lining ofthe vessel, (2) venous stasis, and (3) a change in blood con- stituents attributable to postopcrativc increase in the number and adhesiveness of the patient's platelets. The classical clinical featurcs ofDVT are: . . . Calfswelling Feler . . Sudden dyspnca Tachypnea Chcst pain A patient who has developed DVT should be staied immediately on systemic anticoagulation with clevation of the affected Iimb. lmportant; The most frequent respiratory complications following oral and maxillofacial surgery are: pulmonary atelectasis (mosl often in smokers), aspiration pneumonia /ikely to mani.lest itlitially tu lhe patient's rigllt lwtg), and pulmonary embolus fmosl fr?o.t, originate in lhe deep venous s,,'stems oftlrc lower extremities, especially in nonantbulatory'patients).

Which artery descends on the posterior surface Sphenopalatine artery Greater palatine artery Posterior superior alveolar artery Infraorbital artery

Posterior superior alveolar artery The externaf carotid artery supplies most ofthe head and neck, except for brain (the btain gets its blood supply from the the internal carotid and the veltebrql arleries). The extemal carotid passes through the parotid salivary gland and terminates as the maxillary and superficial tenpo- ral arteries. The superficial artery supplies the scalp. The maxillary artery leaves the infratemporal fossa by passing though the pterygomaxillary fissure into the pterygopalatine fossa. Here it splits up into branches that accompany the branches ofthe maxillary nerve. It supplies the muscles ofmastication, the maxillary and mandibular teeth, the palate, and almost all ofthe nasal cavity. The matrdibular t€eth receive blood from the inferior alveolar artery, which is a branch of the maxillary artery. The maxillary teeth also receive blood from branches ofthe maxillary artery as follows: . Posterior teeth: from the posterior superior alveolar artery . Anterior teeth: from the anterior and middle superior alveolar artedes. Remember: The venous return ofboth dental arches is the pterygoid plexus ofveins. Branches ofthe maxillary artery that accompany the branches ofthe maxillary nerve; l. The posterior superior alveolar artery descends on the posterior surface ofthe maxilla and supplies the maxillary sinus and the maxillary molar and premolar teeth. 2. The infraorbital artery ente$ the orbital cavity thrcugh the inferior orbital fissure. lt ends by emerging on the face with the infraorbital nerve. 3. The greater palatine artery descends through the grcater palatine canal with the greater palatine nerve. tt is distributed to the mucous membrane covering the oral surface ofthe hard palate. 4. Tbe pharyngeal branch passes backward to supply the mucous membrane ofthe roofofthe nasopharynx. 5. The sphenopalatin€ artery passes thrcugh the sphenopalatine foramen into the nasal cavity. It supplies the mucous membrane ofthe nasal cavity.

All of the following are local anesthetics available on north america except Prilocaine Bupivacaine Lidocaine Procaine Mepivacaine Articaine

Procaine Procaine (Novocaine) was, at one time, the most commonly used ester local anesthetic in dentistry Il is thc protolvpe for the ester group oflocal anesthetics but is no longer available in dental cartridgc fo.m. An easy way to identify amide local anesthetics is to rcmember that the drug name contains an i plus crine (lidocaihe, mepi|acaine, and bupivacaine). Estors such as procaine, benzocaine, and tetracaine conlaln no 1. Amide-t] pe local anestheticsi . . Lidocairc Pilocaine . \t,rcaine . (X),locainel: (Citanest) (Septocaine/: \Icpit acatne . Bnpi ac arne . most commonly used has both amide and ester linkages (Carbocaine) I[a rc a i ne) I Eridocaine /Darznestlr removed from the U.S. market in 2002 Ester-tlpe local anestheticsi . . . . Proc i're (Novocaine) P I opoxy caine (Raroc a i ne Bcnzocaine (Monocaine) Tetrac ine TLrpical esters are still commonly used in the practice ofdentistry Most topical local ancsthctic oint- ments and gels contain benzocaine (an ester e.g., Httticaine, Celacaine). Benzocaine gels typically contain I 89 6 - 20% benzocaine. Lidocaine /a ri(rn. EI1LA /ekrecric mixlure o.[ local anesthetic c],ea (Pontocaine) n amide) ls also avallable in two foms for topical applica- ), containsboth lidocaine and prilocaine. -\mides are safe, versatilc, and effective local anesthetics. Ifhypersensitivity to a drug in this group pre- chrdes its use, one of the ester-compound local anesthetics may provide analgesia without adverse effect For patients allcrgic to both esters and amides, diphenhydramine (Benadryl) is good choice Esters are potent local anesthetics slightly different in chemical structure from the amide group. Tetra- caine is most commonly used. Allergic rcactions are far more common with esters' ^ lmportant: The local anesthetics lidocaine and prilocaine are recommended for the pregnant (Class B) patient. For the pregnant used. fcldsr C, patient, articaine, bupivacaine, mepivacaine, and epinephrine can bc Remember: The drug of choice in management ofan acute allcrgic reaction involving bronchospasm (an acule nat rowing oflhe rcspiralory ainray) and hypotension is epinephrine. Notei Alleryic reactions to local anesthetic are usually caused by an antigen-antibody reaction

The following signs: nausea, pallor, cold perspiration, widely dilated pupils, eyes rolled up, and brief convulsions are indicative of a patient having a ? reaction Either of the above None ofthe above Somatogenic Psychogenic

Psychogenic *** A psychogenic reaction is caused by psychological factors rather than physical factors (drugs). Vasovagal s,'rlcope, a psychogenic r€action, is the most cornmonly experienced complication associated with the use oflocal anesthetic solutions. The clinical signs closely resemble those ofshock. These psychogenic reactions readily respond to placing the patient in a supine position. The following drugs, when administered one hour pdor to the dental appointment, are safe and eff€ctive ways to allay the fears ofan apprehensive adult dental patient and possibly avoid a psychogenic reaction in the dental chair: *** . . . . Diazepan\ (Vqlium): 5- l0 mg orally 1PO) Pentobarbital (Nembutal):50- 100 mg orally /POl Secobarbital f^9econal): Promethazine (P,lr 50-100 mg orally (PO) energan): 25 mg orally (PO) Note dosages and route of administration. These drugs are not recomm€nded unless you have experience with them and can handle any complications that may happen from th€ir use. \ote: For a dentist to use "ent€ral sedation" (the use of a pharnracological method that produces a minimally-depressed level o.f consciousness) some states require special training and registration with the stat€. \ote: A somatogenic reaction is the development of a reaction from an organic pathophys- iologic cause.

The buccinator and the superior phryngeal constrictor muscles of the pharynx are attached to each other at the Pterygomandibular raphe Mastoid process Epicranial aponeurosis Genial tubercles on the intemal surface of the mandible

Pterygomandibular raphe On each side, the pterygomandibular raphe extends from the hamulus and passes infe- riorly to attach to the posterior end ofthe mandible's mylohyoid line. It is formed by the union ofthe tendinous ends ofthe superior constrictor ofthe pharynx and the buccinator muscle. Note: As the mandible moves relative to the hamulus, the length ofthe raphe is passively increased. The pterygomandibular raphe is noted in the oral cavity as the pterygomandibular fold. .--.., . L The buccinator muscle is pierced by the needle when performing an inferior l Notegll alveolar nerve block. 'W 2. The deep tendon of the temporalis muscle and the superior pharyngeal constrictor muscle form a V-shaped landmark for an inferior alveolar nerve block. 3. When draining purulent exudate from an abscess of the pterygomandibu- lar space from an intraoral approach, the buccinator muscle is most likely to be incised.

Which component of the TMj hs the most vasculature and innervation? Articular fossa Anterior band of the articular disc Posterior band of the articular disc . Articular eminence . Retrodiscal tissue

Retrodiscal tissue The articular disc (meniscus) is composed of dense fibrous connective tissue, and it is positioned in between the condyle and the fossa, thereby dividing the inferiorjoint spaces. joint The articular disc (nteniscus) vaies inthickness; the thinncr ccntral intermediate zone separates the thicker portions, which are the anterior and posterior bands. The posterior band of the articular disc is the thickest of the two bands, and it is attached with posterior loose connective tissues called retrodiscal tissues (bildminar zone; postefiot attachment). The less thick anterior band of the articular disc is contiguous with the capsular ligament, the condyle, and the superior belll ofthe lateral pterygoid muscle. \ote: The retrodiscal tissue is highly vascularized and innervated, whereas the articular disc for the nosl part is not. Only the extreme periphery of the afiicular disc is slightly innervated.

A patient comes into your dental o{fice complaining of chewing dilficulties. When you ask him to protrude his mandiblen the mandible markedly deviat€s to th€ right. Which muscle, which inserts fibers into the capsule and articular disc of the TMJ, is most likely damaged? Right medial pterygoid muscle Lefl medial pterygoid muscle Right lateral pterygoid muscle

Right lateral pterygoid muscle (with lateral pterygoid injury the mandible will deviate towards the site of injury) The mandible will also deviate toward the side of iniurv with .,{nkylosis ofthe condyle: the most common cause ofTMJ ankylosis is trauma . A unilateral condylar fracture The mandible will deviate away from the affected side with: . Condylar hyperplasia: malocclusion is also a common occurrence with this injury and leJi) acting together are the prime protractors of the mandible. Important: In addition to opening and protruding, the lateral Remember: The lateral pterygoids (right pterygoids move the mandible from side to side, For right lateral excursive movements, the left lateral pterygoid muscle is the prime mover and vice versa. A patient who sustained a subcondylar fractare (unilateral condylar left side would be unable to deviate the mandible to the right (as stated qbove the mandible v,ill deviate to the side o/ injury with a unilateral condylar fracture) fracture, u'ottlrl not be able to deviate the mqndible to the right) This is normally treated by a closed proc€dure involving intermaxillary fixation. This procedure immobilizes the concomitant fractures and conects the displacement ofthe jaws on lhe this patient associated with the condylar ftacture thereby conecting the shift ofthe midline toward the side ofthe fiactured condyle and the slight prematue posterior occlusion on that side.

The greater platine foramen is most frequently located distal to the apex of the maxillary: First molar Second premolar Second molar Canine

Second molar The greater palatine foramen is generally located halfway between the gingival margin and mid- line ofthe palate, approximately 5 mm anterior to thejunction ofthe hard and soft palate (vibrat- ing line) distal to the apex ofthe maxillary second molar The hard palate is perfonted by the following foramina; . The incisive foramen, posterior to the maxillary incisors, which transmits the nasopalatine nerves and the terminal branches ofthe sphenopalatine artery . The greater palatine foramen, is most Iiequently located distal to the maxillary second molar, which transmits the greater palatine vessels and nerve . The lesser palatine foramen, lesser palatine vessels and nerve Nerves of the palate: . j ust poste.ior to the greater palatine foramen, which transmits the Sensory Inneryation to lhe palate: is supplied by the m^xillary (CN I/-2) nerve. The ante- rior part ofthe hard palate is supplied by the nasopalatine nerve which passes through the in- cisive foramen. The posterior part ofthe hard palate is supplied by the gr€ater palatine nerve which passes through the greater palatine foramen. The soft palate is supplied by the lesser pala- tine nerve which passes though the lesser palatine foramen. . Motor Innervation: the tensor veli palatini is innervated by a muscular branch from the mandibular division ofthe trigeminal nerve ryngeal plexvs (motor pottion from fCN Z/. All othermuscles are innervated by the pha- the vagus nerve and cranial part of lhe accessory nene), The greater palatine block or GP block is useful for dental procedures involving palatal soft tis- sues distal to the maxillary canine. This maxillary block anesthetizes the posterior portion of the hard palate, anteriorly as far as the maxillary first premolar and medially to the midline. ater (anterior) palatirre nerve as it passes anteriorly between the sofi tissues and bone of the hard palate. Target area: the gre The nasopalatine nerve block anesthetizes the anterior portion ofthe hard palate (soft and hard tis.sre,r) from the mesial ofthe right first prcmolar to the mesial of the left fiIst premolar. Target area: incisive foramen, beneath the incisive papilla.

During extrrction ofa madllary third molar, you realize the tuberosity has also been extracted. Whats the proper treatment in this case? Remove the tuberosity fiom the tooth and reimplant the tuberosity Smooth the sharp edges ofthe remaining bone and suture the remaining soft tissue No special treatment is necessary None ofthe above

Smooth the sharp edges ofthe remaining bone and suture the remaining soft tissue A fracture ofthe maxillary tuberosity most commonly results from extraction ofan erupted maxillary third molar -or a second molar if it happens to be the last tooth in the arch. lf the tuberosity is fractured but intact, it should be manually repositioned and stabilized with sutues. The complications most often seen after extraction of an freestanding, isolated maxillary molar are: . . Fractwe ofthe tuberosity Alveolar process fiacture Important: "Beware ofthe lone molar'r- it is often ankylosed to the bone. Remember: The ankylosed tooth emits an atypical, sharp sound on percussion. Key point to remember: Tuberosity ftactures may occur and should be treated at the time of sugery Ifthe operator is unable to do this he / she must arrange an immediate referral. l. For denture construction, at the correct v€rtical dimension, the distance from tho crest ofthe tuberosity to the retomolar pad should equal at least I cm. 2. Ifthere is inadequate intermaxillary distance at the tuberosity a tuberosity reduction can be performed to remove excess tuberosity. An elliptic incision is made over the tuberosity and carried down to bone. This wedge is resected, The buccal and palatal tissues axe undermined subperiosteally. Submucous wedges are re- moved flom each flap and the wound is closed. This decreases the vertical and hor- izontal dimensions of the tuberosity.

The primary action of local anesthetics in producing a conduction block is to decrease the permeability of the ion channels to Calcium ions Chloride ions Potassium ions Sodium ions

Sodium ions Local anesthetics selectively inhibit the peak permeability of sodium, whose value is normally about five to six times greater than the minimum necessary for impulse conduction. The following sequence is a proposed mechanism of action of local anesthetics: l. Displacement ofcalcium ions from the sodium channel receptor site, which permits... 2. Binding oflocal anesthetic molecule to this receptor site, which thus produces... 3. Blockade ofthe sodium charmel, and a... 4. Decrease in sodium conductance, which leads to... 5. Depression oflhe rate ofelectrical depolarization, and a... 6. Failure to achieve the threshold potential level, along with a... 7. Lack ofdevelopment ofpropagated action potentials, which is called... 8. Conduction blockade The mechanism whereby sodium ions gain entry to the axoplasm ofthe nerve, thereby initiating an action potential, is altered by iocal anesthetics. The nerve membrane rcmains in a polarized state because ionic rnovemcnts rosponsible for the action potential fail to develop. Nerve block produced by local anesthetics is called a nondepolarizing nerve block. *** l. Local anesthetics reversibly block nerve impulse conduction and produce reyersible loss of sensation at their administration site. The side of action of local anesthetics is at the lipoprotein sheath ofthe nerves. 2. Local anestbetics are clinically effective on both axons and free nerve endings. 3. Important; Small, myeliDated nerv€ libers which conduct pain and tempenture sensations, are affected first, followed by touch, proprioception, and skeletal muscle tone. 4. Emergenc€ from a local anesthetie nerve block follows the same diffusion pattems as induction does; however, it does so in reverse order. 5. Recovery is usually a slower process than induction beaause the anesthetic is bound to the drug receptor site in tbe sodium channel and therefore is released more slowly than it is absorbed. 6. Potassium, calcium, and chloride conductance's remain unchangcd.

A dentist is performing a routine restoration on the left mandibular first molar, He is giving an inferior alveolar nerve block injection, where he deposits anesthetic solution right next to the Iingula and mandibuhr foramen. Which ligament is most likely to get damaged? Sphenomandibular ligament Temporomandibular ligament Stylomandibular ligament

Sphenomandibular ligament Thc sphenomandibular and stylomandibular ligaments are considered to be accessory ligaments. The former is attached to the lingula of the mandible and the latter at the angle of the mandible. These ligaments are responsible for limitation ofmandibular movements (thet linit excessive opening). Note: The sphenomandibular ligament is most oftcn danaged in an inferior alveolar nerve block. called the lateral liganert) runs from the articular eminence to the mandibular condyle. It provides lateral reinlbrcement for the capsule. This ligament The temporomandibular ligament fabo prevents posterior and inferior displacement ofthe condyle (it is the rlain srabilizing liganrent oJ the TMJ). Notei This ligament keeps the head of the condyle in the mandibular fossa if the condyle is fractured. Collateraf figaments (medial and lateral) also referred to as "discal ligaments," are Iigaments that arise from the periphery ofthe disc, are attached to the medial and iateral poles ofthe condyle re- spectively, and stabilize the disc on the top ofthe condyle. These ligaments rcstrict movement of the disc away from thc condyle during function. Note: They arc composed of collagenous connective tissuc: thus they do not strelch.

According to Guedells stages of anesthesia the proper use of nitrous oxide acheives which level of anesthesia Stage I Stage II Stage III Stage IV

Stage I Geudel's Stages of Anesthesia: St|ge | (amnesia and analgesia)': begins with the administration of anesthesia and continues to the loss of consciousness. Respiration is quiet, though sometimes irregu- lar. and reflexes are stillpresent. Stage ll (delirium and excitement):begins with the loss ofconsciousness and includes the onset oftotal anesthesia. During this stage the patient may move his limbs, chatter incoherently, hold his breath, or become violent. Vomiting with the attendart danger of aspiration may occur. The patient is brought to Stage III as quickly and as smoothly as possible. Stage III (surgical anesthesia): begins with the establishment ofa regular pattern of breathing, total loss ofconsciousness and includes the period during which signs ofres- piratory or cardiovascular failure first appear. This stage has four planes. Stage IV (premortem)i signals danger. This stage is characterized by pupils that are maximally dilated and skin that is cold and ashen. Blood pressure is extremely low, often unmeasurable. Cardiac arrest is imminent. Rememtrer: The eyes appear geatly enlarged in size and nonreactive to bright light when functional circulation to the brain has stopped.

The carotid sheath contains all of the followlng EXCEPT one, Carotid artery Sympathetic trunk Jugular vein Vagus nerve

Sympathetic trunk ***The carotid sheath does not contain the sympathetic trunk, which lies posterior to the carotid sheath and anterior to the prevertebral fascia. The carotid sheath is located at lhe lateral boundary ofthe retropharyngeal space at the level ofthe oropharynx on each side ofthe neck deep to the stemocleidomastoid muscle. It extends from the base ofthe skull to the first rib and sternum. It contains the carotid arteries, the jugular vein, and the vagus nerve. Within the carotid sheath, the vagus nerve (CN-! lies posterior to the conrnon carotid artery and intemaljugular vein. The facial vein unites with the retromandibular vein below the border ofthe mandible and empties into the main venous structure ofthe neck, the internal ternal jugular jugular vein descends through the neck within the carotid sheath and unites be- hind the sternoclavicular joint vein. The in- with fte subclavian vein to form the brachiocephalic vein. The brachiocephalic veins (ngi t and lefi) unite inthe superior mediastinlun to form the superior vena cava, which retums blood to the right atrium ofthe heart.

Which oral landmark marks the opening of the submandibular duct Lingual frenum Nasolacrimal duct Parotid raphe Sublingual caruncle

Sublingual caruncle The submandibular glatds (formerly celled the submaxillary glands) arc located in the submandibular triangle ofthe neck and the floor ofthe oral cavity. The submandibular duct (Wharton's duct) is a long duct that travels along the anterior floor of the mouth. The duct opens into the oral cavity at the sublingual caruncle, a small papilla near the midline ofthe mouth floor on each side ofthe lingual fienum. Clinically, the gland is effectively palpated in- fe or and posterior to the body of the mandible, moving inward from the inferior border of the mandible near its argle as the patient lowers the head. Note: The submandibular gland is a mixed gland, secreting both serous and mucous saliva, but predominantly serous secreting. The submandibular glands are innervated by efferer,t (paras4pathetly' secretomotor fibers from the facial nerve, which run in the chorda tympani and in the lingual newe (branch of Z-3) and synapse in the submandibular ganglion. Note: This is the same as the sublingual glands. The blood supply comes from branches of the facial and lingual arte es. The veins drain into the facial and lingual veins. The lymph vessels drain into the submandibular and deep cewical lymph nodes. Important: During its course, Wharton's duct is closely related to the large lingual nerve *.hich eventually crosses over it. This is important because if you incise the mucous mem- branes of the floor of the mouth, depending on where you cut, you may expose the lingual nerve, Wharton's duct, and the sublingual gland. ,n;4 '%# l. To expose the duct intraorally, only mucous membrane needs to be cut through. 2. L).rnphadenopathy is the most common cause ofswelling ofthe tissues in the sub- mandibular triansle.

Which lymph nodes directly recieve lymph from the anterior 2/3rds of the tongue (except the tip) Submental lymph nodes Submandibular lymph nodes Parotid lymph nodes

Submandibular lymph nodes The deep cewical lymph nodes ar€ located along the length ofthe intemal jugular vein on each side ofthe neck, deep to the stemocleidomastoid muscle. The deep cervical nodes extend from the base ofthe skull to the root ofthe neck, adjacent to the pharynx, esophagus, and trachea. The deep cer- vical nodes are further classified as to their relationship to the stemocleidomastoid muscle as beins superior or inferior. The deep cervical lymph nodes are responsible for the drainage of most of the circular chain of nodes, and receive direct efferents from the salivary and thyroid glands, the tongue, the tonsil, the nose, th€ pharynx, and the larynx. All these vessels join together to form the trunk. This vessel drains into either the thoracic duct on the left, the right lymphatic duct on the right, or independently drains into either the intemal velns. Some regional groups of lymph nodes: . jugular, jugular lymph subclavian, or brachiocephalic Parotid lymph nodes - receive lymph from a strip of scalp above the parotid salivary gland, from the anterior wall ofthe extemal auditory meatus, and from the lateral parts of the eyelids and middle ear. The efferent lymph vessels drain into the deep cervical nodes. . Submandibular lymph nodes - located between the submandibular gland and the mandible; receive lymph liom the front of the scalp, the nose, and adjacent cheek; the upper lip and lower lip (ercept the center p.trt); tlrc paranasal sinuses; the maxillary and mandibular teeth the mandibular incisorsl; the aDterior two-thirds of the tong\e (except fercepl the tip); the floor ofthe mouth and vestibule; and the gingiva. The eferent lynph vessels drain into the deep cervical nodes. . Submental lymph nodes - located behind the chin and on the mylohyoid muscle; receive lymph from the tip of the tongue, the floor of the mouth beneath the tip of the tongue, the mandibular incisor teeth and associated gingiva, the center part of the lower lip, and the skin over the chin. The eflerent lymph vessels drain into the subrnandibular and deep cervical nodes.

Anesthesia performed with general anesthetics occurs in four stages which may or may nor be observable because they occur very rapidly. Which stage is the one in which skeletal muscles relax and the patients breathing becomes regular. Analgesia Excitement Surgical anesthesia Medullary paralysis

Surgical anesthesia Stage One (Anqlgesia) i The patient experiences analgesia or a loss ofpain sensation but remains conscious and can carry on a conversation. Note: The best monitor ofthe level ofanalgesia is the verbal response. . Stage Two (Exciteuent): The patiefimay experience delirium or become violent. Blood pres- sure rises and becomes iregular, and brcathing rate increases. This stage is t)?ically bypassed by administering a barbiturate, such as Methohexital or Thiopental, before the anesthesia. . Stage Three (^laryical Anesthesio): During this stage, the skeletal muscles relax, and the pa- tient's breathing becomes regular. Eye moyements slow, then stop, and sugery can begin. . Sttge Four (Medullary Paralysis): This stage occurs ifthe respirctory centers in the medulla oblongata ofthe brain that control breathing and other vital functions cease to function. Death can result ifthe patient cannot be r€vived quickly. This stage should never be reached. Careful con- trol ofthe amounts ofanesthetics administered Drevent this occurrence. l. The medulla is the last area ofthe brain to be depressed during general anesthesia. This area is the most vital part of the brain and contains lhe cardiac, the vasomotor, and respiratory centers ofthe bmin. 2. The most reliable sign of "oxygen want" while monitoring a patient dudng gen- eral anesthesia is an increased pulse rate, Cyanosis may also be present. 3.The emeryency most frequently experienced during outpatient general anesthesia is respiratory obstruction. 4. The best anesthetic techlique used in oral suryery to avoid aspiration of blood or other debris when a patient is under general anesthesia is endotracheal intubation with pharyngeal packs. 5. A patient with an acute respiratory inf€ction is contraindicated for general anes- thesia. 6. The eyes are taped shut priorto draping a patientbefqre surgery to preyent corneal abrasion.

After receiving an injection of a local anesthetic containing 2% lidocalne with 1:100,000 epinephrine, the patient loses consciousness. Which of the following is the most probable cause? Hyperventilation syndrome . Acute toxicity Allergic response Syncope

Syncope *** Caused by transient cerebral hypoxia Anxiety-induced events are by far the most common adverse r€action associated with local anesthetics in dentistry. These may manifest in numerous ways, the most common ofwhich is syncope, In addition, they may present with a wide variety of symptoms, including hyperventilation, nausea, vomiting and altemtions in heart rate or blood pressure. Psychogenic re- actions are often misdiagnosed as allergic reactions and may also mimic them, with signs such as urticaria, edema and bronchospasm. Proper management of syncope: . . Place patient in supine position with feet slightly elevated Establish airway (head tilt/chin lift) @endelenburg - Administer 1007o oxygen via face mask. 02 is indicated fbr the treahnent ofall types ofsyncope except for hlTrerventilation syndrome. . Monitor vital signs and support patient . - Pupils may dilate from brain not getting oxygen. Maintain your composure. Apply cool, wet towel to patient's foreh€ad. . Follow-up treatment - Determine lactors crusing unconsciousness. Remember: Hyperyentilation in an anxious dental patient leads to carpopedal spasm /a spasm ofthe hand, thumbs, foot, or toes).

The most common cause of loss of caonciousness in a dental office is Anaphylaxis Syncope Heart attack Seizure

Syncope S.u-ncope is thc most common adverse reaction associated with administration of local anesthesia. Remember: It often occurs when upright, though can occur when sitting. It u'ill never occur when lying. The patient may complain offeeling generalized warmth rvith nausea and palpitations, Thc initial event in a vasovagal syncope episode is the stress-induced release of in- creased amounts of catecholamines that causes the following: a decrease in peripheral \'ascular resistance, tachycardia, and sweating. .{s blood pools in the periphcry a drop in blood prcssure appears, with a corresponding decrease in cerebral blood flow. The patient will then complain offeeling dizry or weak. Compensatory mechanisms attempt to maintain adequate blood pressure, but they soon fatigue, which lcads to vagally mediated bradycardia. Once the blood pressure drops bclou lcrels necessary to sustain consciousness. syncopc occurs. Place the patient in a supine position with the feet elevated (Trendelenburg posilion), monitor vital signs, tight clothing should be loosencd and a cold compress placed on the forehead. Oxygen 3-4 L/minute should be given via nasal cannula. Important: The single most important drug to use in any medical emergency, includ- ing chronic obstructive pulmonary disease, is oxygen. Note: The primary ailway hazard for an unconscious dental patient in a supine position is tonsue obstruction. Remember: Head titt/chin lift.

A person who has been on suppresive doses of steroids will Never regain full adrenal cortical function Take as much as a year to regain full adrenal cortical function Take as little as a week to regain full adrenal cortical function Take usually a couple of days to regain full adrenal cortical function

Take as much as a year to regain full adrenal cortical function The following guidelines may help determine if a patient's adrenal function is suppressed, however, ifany doubt €xists, consult the patient's physician before performing surgery. Some Guidelines: . People on smalf doses (5 mg Prednisone/day) will have suppression when they have been on the regimen for a month. . People taking equivalence of 100 mg cortisol/day (20-30 mg Prednisone/da1) wrll have abnormal cortical function in a week. . Short-term therapy function. . (1-3 days) ofeven high dose steroids will not alter adrenal cortical A person who has been on suppressiye doses of steroids will take as much as a year to regain full adrenal cortical function. Patients with a&enal insu{ficiency are hyperpigmented. This is most noticeable on the buccal and labial mucosa, although other areas such as the gingiva may be involved. The hyper- pigmentation is a result of hypersecretion of ACTH, which can stimulate melanocytes to produce pigment. Patients rvith decreased adrenal gland hormone production experience weakness, weight loss, onhostatic hypotension, nausea, and vomiting. Patients with severe adrenal insufficiency can- not increase steroid production in response to stress and in extreme situations may have car- diovascular collapse. It is important that an adrenally insufficient patient have adequate steroid replacement, since the stress oforal surgery can precipitate adrenal crisis. ln adrenal crisis, an intravenous or intramuscular injection ofhydrccortisone must be given immediately. Supportive treatment of low blood pressure with intravenous fluids is usually necessary. Hospitalization is required for adequate treatment and monitoring.

Postoperative hypotension is usually due to the effect of Liver failure The anesthetic or analgesics on the myocardium Transfusion reactions A fat embolism

The anesthetic or analgesics on the myocardium *** Leading to myocardial depression. Common causes of postoperative hypotension: . Intravascular hypovolemia . Rewarming vasodilation 'Hypothyroidism . Myocardial depression *** Possible treatment options include: . . . Elevation ofthe lower extremities Administration ofcarefully monitored fluid boluses Administration of vasopressors (e.g., ephedrine) The treatment is n rc n (a narcotic antagonist/ if hypotension is due to narcotics. Use aftopine (qn anticholinergic) ifbradycardia is present. Note: Postoperative [ypgltension is most often due to post-op pain. Treat with narcotics and sedatives. Oth€r common causes include: . . Hypercapnia Anxlety . . Overdistention of the bladder HvDoxia

In which of the following areas is the trigeminal ganglion located Superior to the deep lobe ofthe submandibular salivary gland Posterior surface ofthe ma-rillary tuberosity ofthe maxilla . Anterior to the infraorbital foramen ofthe maxilla . The apex of the petrous part of the temporal bone in the middle cranial fossa

The apex of the petrous part of the temporal bone in the middle cranial fossa The rrigeminal newe emerges from the anterior surface of the pons by a large sensory and a small motor roor. Ihe motor root lying medial to the sensory root. The nerve passes forward out of the postedor cranial fossa, below the superior petrosal sinus, and carries with it a pouch derived from the meningeal la)er ofdura mater. On reaching the depression on the apex ofthe petrous part ofthe temporal bone in the middle cranial fossa, the large sensory rcot expands to form the trigeminal ganglion. The motorroot of rhe rigeminal nerve is situated below the sensory ganglion and is completely separate from it. The ophthalmic, maxillary and mandibular nerves arise from the anterior border ofthe ganglion. Somatic sensory cell bodies ofthe ganglion,s . Ophthalmic division 1f-1) sensory libers enter the: to supply general sensation to the orbit and skin of face above eyes . \Iaxillary division (Y-2) to supply general sensation to rhe nasal cavity, maxillary teeth, palate, and skin over maxilla . \landibular division fZ-3) to supply general sensation to the mandible, TMJ, mandibular teeth, floor ofmouth, tongue and skin ofmandible The axons of rhe neurons gnter the pons through the sensory rcot and terminate in one of the three nuclei ofthe trigeminal sensory nuclear complex: \ote: Proprioceptive fibers fiom muscles and the TMJ are found only in the mandibular division. The cell bodies of proprioceptive first order neurons arc found in the mesencephalic nucleus, not the mgeminal ganglion. The TMJ, as is the case with alljoints, receives no motor innervation. The muscles rhat move the joint receive the motor innervation. Branchiomeric motor libers innervate the temporalis, masseter, medial and lateral pterygoid, anterior belly of the digastric, mylohyoid, tensor tympani, and tensor veli pa,latjni (palati).

Renal dialysis produces concern as to when best to dentally tret this patient. A concern is the use of heparin in the dialysis process and its effect on oral bleeding. When is the best time to treat the dialysis patient? The day before dialysis The day ofdialysis The day after dialysis Two days before dialysis

The day after dialysis End-stage renal disease (ESRD) rs a condition in which there is a permanent and almost complete loss of kidney function. The kidney functions at less than I 0% of its normal capacity. [n end-stage renal disease, toxins slowly build up in the body. Normal kidneys re- move these toxins /i.e., urea and creatinine) from the body through urine. In chronic renal disease there is a slow, progressive decline in kidney functiot (low glomerular ICFRI andfall in uri e output). Creatinine clearance is a measure ofGFR: . Normal range: Male: 120 +/- 25 ml/min Female: 95 +/- 20 ml/min *** End-stage renal disease: GFR Patients u,ith ESRD: . . . *** Are often on steroid therapy Are more susceptible to post-op infections Have an increased tendency to bleed < l0 ml/min when oral surgical procedures are undertaken on these patients, meticulous attention to good surgical technique is necessary to decrease the risks ofexcessive bleeding and infection. Some important points to remember when treating patients with renal insufltciency and rhose on hemodialysis: . \er er measure the patient's blood pressure on the ann where the dialysis shunt has been created . . Avoid the use ofdmgs that are metabolized or excreted by the kidney Ar oid the lollowing analgesics: aspirin, acetaminophen, NSAlDs, meperidine, and mor- phine . . Perform oral surgery the day after dialysis Consult physician for possible prophylatic antibiotics

In preparing the edentulous mandible for dentures each of the following may be safely excised except one: A labial frenum . A lingual frenum The mylohyoid ridge The genial tubercles An exostosis

The genial tubercles The genial tubercles are situated on the lingual surface of the mandible at a point about mid*ay between the superior and inferior borders. There are four of them, two ofwhich are situated on each side and adjacent to the symphysis. Although usually relatively small, they may be fairly large and extend outwaxd from the surface as spinous processes. These tubercles are the area of muscle attachment for the suprahyoid muscles. Important: Ifthe genial tubercles were removed, the tongue would be flaccid. l. When removing the mylohyoid ridge, be careful to protect the lingual nerve. 2. When removing a mandibular exostosis (mandibular torus) it is recom- mended that an envelope flap design, which has no vertical components, be used.

Which tooth has a root thrt is not consistently innervated by the PSA nerve? The maxillary first molar The maxillary second molar The maxillary third molar AIl of the above

The maxillary first molar \'hen used to achieve pulpal anesthcsia, thc PSAnerve block is eflective for thc maxillary third, second, and first molars in 77olo to 10070 ofpatients. Howevet the mesiobuccal root ofthe ma,\illary first molar is not consistenrly innervated by the PSA n€rve. In approximately 28% ofpatients the middle superior ah eolar nerve provides sensory ilnervation to the mesiobuccal root ofthe maxillary first molar. There_ fore. if anesthesia ofthis tooth for either restomtive dcntistry or extraction is requircd, an infiltration in- jection also should be performed over the second premolar tooth. Note: Patients experience few subjective signs ofanesthesia after receiving a poste or superior alveolar nerve block, as compared to an inferior alveolar ner'-eblock (humb lip). The risk ofa potential complication also must be considercd whencver the PSAblock is used. Insertion ofthe needle too far distally may lead to a tempo..ary (10 position) to 14 days) unaesthetic hematoma. As a means ofdecreasing the risk ofhematoma formation afler a PSA nerve block, the use of a "short" dcntal needle is recommended for all but the largest ofpatients. One must remember to aspirate seveial times be- fore and during drug deposition during the PSAnerve block to avoid inadvertent intravascular injection Important: Ifa patient's face becomes distended and swollen after a posterior superior alveolar nerve block, the following treatment is recommended: . . Place cold packs and pressure on the affected side Explain to the patient that he/she may become black and blue on that sids L Gauge ofa needle refers to the diameter ofthe lumen ofthe needle: the smaller the num- ber, the greater the diameter ofthe lumen. A 30-gauge needle has a smaller intemal diame- gauge: 25-gauge, red; 27-gauge, yellow; and 3O-gauge, blue. ter than a 25-gauge needle. In the United States, ncedles are color-codedby 2. Positive aspiration is directly correlated to needlc gauge. 3. Larger-gauge needles (i.e., 25-gauge) have distinct advantages over smaller ones: . . Less deflection as the needle passes through the tissues This leads to greater accuracy in needle insertion and, hopefully, to incrcascd success lales . Largcr-gauge needles do not brcak as o{ien Important: The 25-gauge needle is the preferred needle for all injections presenting a high risk ofposjtive aspiration.

The parotid gland receives parasympathetic secretomotor fibers from the inferior salavary nucleus of the Facial nerve Trigeminal nerve Vagus nerve Glossopharyngeal nerve

The nerve fibers pass to the otic ganglion via the tympanic branch ofthe glossopharyngeal nerve and the lesser petrosal nerve. Postganglionic parasympathetic fibers reach the parotid gland via the auriculotemporal nerve, which lies in contact with the deep sur- lace ofthe gland. Note: Postganglionic sympathetic fibers reach the gland as a plexus of nerves around the extemal carotid artery The parotid gland is the largest ofthe major salivary glands and is entirely serous in se- cretion. The parotids are located below andjust anterior to the ear. The gland's capsule is from the deep cervical fascia. About 750% or more ofthe parotid gland overlies the mas- seter muscle. the rest is retromandibular. The parotid gland is drained by Stenson's duct, which forms within the deep lobe and passes from the anterior border of the gland across the masseter muscle superficially, through the buccinator muscle into the oral cavity opposite the maxillary second molar. The external carotid artery and its terminal branches within the gland, namely, the su- perficial temporal and the maxillary arteries, supply the parotid gland. The lymph vessels drain into the parotid lymph nodes and deep cervical li,mph nodes. . Notoi: , .,: :#;{ 1. Mumps is a viral disease of the parotid gland. Parotitis is the inflammation ofthe parotid gland. 2. Von Ebner's glands are the only other adult salivary glands which are purely serous. 3. Although it passes through the parotid gland, the facial nerve do€s not pro- vide any innervation to it.

All ofthe following are rersons that vasoconstrictors are included in local anesth etics EXCEPT one. Which one is th e EXCEPTIOM They prolong the duration ofaction ofthe local anesthetic They reduce the chance ofan allergic reaction to the local anesthetic They reduce the toxicity because less local anesthetic is necessary They reduce the rate ofvascular absorption by causing vasoconstriction . They help to make the anesthesia more profound by increasing the concentrations ofthe local anesthetic at the nerve membrane

They reduce the chance ofan allergic reaction to the local anesthetic *** This is false. Vasoconstrictors are invaluable to local anesthesia in dentistry. There are clear indications for their use, ofwhich improving the depth and duration ofanesth€sia are the most important. Without them, local anesthetics haye a very short duration ofaction intraorally. Vasoconstric- tion is more important for infiltration techniques in vascular sites than it is for mandibular blocks. The presence of a vasoconstrictor may also reduce systemic toxic effects and can provide hemostasis. The most common agent for this purpose is epinephrine, which is avail- able in fonnulations of l:50,000 (0.02 rng/ml), l:100,000 10.01 mg/ml) and l:200,000 (0.005 mg/mL). There are three main adrenergic receptor subclass€s that vasoconstrictors interact with on car- diovascular tissue in the human body. These are classified as alpha receptors alpha-2),beta-l receptors, and beta-2 receptors. Alpha receptors are densely located on arte- fioles in the skin and mucous membrunes. Stimulation of these receptors leads to vasocon- striction through activation ofG proteins and subsequent opening ofcalcium channels. Beta- I receptors are located on cardiac tissue, and stimulation olthem leads to an increase in heart chronotropr) and aD increase in contraction force (positive i otropy), Beta-2 rcceptors, Iike alpha receptors are located primarily in vascular beds. However, these receptors rate (posilive are located primarily in vascular beds traversing skeletal muscle. when stimulated, beta-2 re- cepto$ activate adenylate cyclase, leading to vasodilation. Epinephrine is the more potent than levonordeliin. Its affrnity for alpha versus beta receptols is roughly equivalent (50:50). Thus, although the primary event that occurs at the site ofin- jection fbot& beneath the oral mucosa is vasoconstriction, the relatively low systemic levels achieved after dental local anesthetic injections can cause increases in heart rate and cardiac output, as u,ell as peripheral vasodilation in skeletal muscle beds. Note: Levonordefiin is less potent than epinephrine, its receptor affinity is 759/o alpha and2'%obeta. As noted earlier' local anes- thetics containins levonordefrin have become impossible to obtain.

Which of these barbiturates can be classilied as an ultra-short-acting compound? Amobarbital Thiopental Phenobarbital Pentobarbital

Thiopental Barbituates exhibit a dose-dependent central nervous system depression with hypnosis and amnesia. Barbiturates are very lipid soluble, which results in a rapid onset ofaction. They are used most often for induction ofanesthesia because thev oroduce unconsciousness in less than 30 seconds. Barbiturates inhibit depolarization ofneurons by binding to the GABA receptorc, which en- hances the transmission ofchloride ions. Note: Barbiturates are potent cerebral vasoconstric- tors resulting in decreases in cerebral blood flow, cerebral blood volume, and intracranial pressure (1CPl. Ultrashort-acting barbiturates : . Thiopental (Pentothal) . . Thiamylal (Surttal) Methohexrtal Short-acting barbiturates : . . P entobarbital Secobarbrtal ( B rev i t a I ) (Nembutal) S ec ona l) Interm€diate-acting barbiturales: . . ( Amobatbital (Amytql) Butabarbital Long-acting barbiturates: . (Fioricet, Fiorinql) Phenobarbital (Luminal): generally not used in oral surgery Important: Barbiturates are contraindicated in patients with respiratory disease or those \\ ho are pregnant. \ote: Phl"sical dependence is likely to develop with barbiturates ifabused. The dependence has a strong psychological as well as physical basis. Sudden withdrawal from high doses can be fatal.

All of the following a true about suturing technique except The needle should be perpendicular when it enten the tissue Sutures should be placed at an equal distance from the rvoun d margin (2-3 mm) and at equal depths Sutures should be placed from mobile tissue to thick tissue Suttrres should be placed from thin tissue to thick tissue Suhfes should not be over-tightened Tissues should be closed under tension Sutures should be 2-3 mm apart The suture knot should be on the side ofthe wound

Tissues should be closed under tension *** This is false; sutures should not be over-tightened or closed under tension. The interrupted suture is the most common suture method. Because each suture is in- dependent, this procedure offers strength and flexibility in placement. Due to this advantage, if one suture is lost or becomes loose, the integrity of the remaining sutures is not compromised. The major disadvantage is the time required for placement ofthis pattem of sutures. (See./igure #1 below) Advantages ofa continuous pattern or method /See/igri . Ease and speed ofplacement . Distribution oftension over the whole suture line . A more watertight closure than the interrupted pattem or method

A history of rheumatic fever, IV drug abuse or heart murmur should alert a dentist to the possibility of Diabetes mellitus AIDS Valvular disease End stage renal disease

Valvular disease Important: Patients with valwlar heart disease are also at risk for bacterial endocarditis. R]leumatic fever is a sequela ofa previous Group A , beta hemolytic streptococcal infection, usually ofthe upper respimtory tract. The disease involves the heart,joints, centml newous sys- tem. skin, and subcutaneous tissues. lt is characterized by an exudative and proliferative in- flammatory lesion of the connective tissue, especially that ofthe heart, and subcutaneous tissue. joints, Hean inflammation (carditis) drsappears gradually, usually within five months. However, it ma) permanently damage the heart valves, resulting in rheumatic heart disease. The valve benr een the left atrium and ventdcle (mitral valve) is most commonly damaged. \ote: The pulmonary valve is rarely involved. Remember: A heart murmur may have no pathological significance or may be an important clue to the presence of valvular, congenital, or other structural abnormalities ofthe heart.

The recommended gas combination dose for concious sedation is 50% oxygen; 50% nitrous oxide 60% oxygen;40% nitrous oxide 40% oxygen; 60% nitrous oxide 30% oxygen; 70% nitrous oxide Varies according to the patient response

Varies according to the patient response The dose ofthe gas combination for conscious sedation is variable and is based on the patient re- sponse. The maximum nitrous oxide limitation is 60010 nitrous oxide and 40olo oxygen. Nitrous oxide is a weak anesthetic and is used with other agents, such as thiopental, to produce surgical anesthesia. It has the fastest induction and recovery and is the safest because it does not slou breathing or blood flow to the brain. Nitrous oxide has a low blood-to-gas partition coe{Ticient (0.46) and therefore low solubility. It can leave the blood and enter air-filled cavities 34 times more quickly than nitrogen can leave the cav- ity to enter the blood. The use ofnitrous oxide can increase the expansion ofcompliant cavities, such as a pn€umothorax, bowel gas in a bowel obstruction, and an air embolism. Importantr The oral and maxillofacial surgeon needs to be cautious when keating the recent hauma patiett (e.g., motorvehicle accident victim). An asymptomatic, undiagnosed closed pneumothorax can double in size in l0 minutes after the administration of 70%o nitrous. Nitrous oxide sedation should be postponed in patients with gashointestinal obstructions, middle ear disturbances, and, possibly, sinus infections.

Epinephrine and levonordefrin are added to local anesthetics because of their Ability to increase the potency of the local anesthetic Abilify to decrease the pain (burning) caused by the injection of the local anesthetic Vasoconstrictive properties Ability to decrease the possibility of an allergic reaction to the local anesthetic

Vasoconstrictive properties Vasoconstrictors (i.e. , epinephrine and levonord.eJrin) are added to local anesthetics because oftheir vasoconstrictive propenics. Vasoconstriction at the site ofinjection is beneficial because it limits the up- take ofthe anesthetic by the vasculature, thereby incrersing the duration ofthe anesthetic and dimin- ishing systemic elTects (redueing systetuic toxicity). Notet The use of a vasopressor-containing local aneslhetic also may actually be responsible for the sensation ofbuming on injection. The addition ofa vasopressor and an antioxidant (sodium bisufite) Iowers the pH ofthe solution to between 3.3 and 4, sig- nificantly more acidic than solutions not containing a vasopressor (pH about 5.5). Patients are more likely to feel the buming sensation with these solutions. Note: Malamed's book states that "local anes- thetics containing the vasoconstrictor levonordefrn Qleo-Cobefrir/ Uune 2004)". lipid solu- have become impossible to obtain Important: To minimize the likelihood ofintravascular injection, aspiration should be performed be- forc the local anesthetic solution is injected. Ifblood is aspirated, the needle must be repositioned until no retum ofblood can be elicited by aspiration. Adverse reactions following the administration ofa local anesthetic are, in general, dose-related and may r€sult from high plasma levels caused by excessive dosage, rapid absorption or unint€ntional in- travascular injection. Systemic toxicities of local .nesthetics: Initial clinical signs and symptoms of mild to moderate tox- icity include: talkativeness, apprehension, excitability, sluned speech, dizziness and disorientation. The signs and symptoms ofsevere toxicity include: seizures, respiratory depression, coma, and death. Important: The excitatory manifestations may be very briefor may not occur at all, in which case the first manifestation oftoxicity may be drowsiness merging into unconsciousness and respiEtory arrest Remember: Cardiovascular manifestations are usually depressant and are characterized by brady- cardia, hypotension, and cardiovascular collapse, which may lead to cardiac arrest. Note: In local anesthesia, the depression ofrespiration is a manifestation ofth€ toxic effects ofthe solution. L For a normrl heafthy (AM I) p^tient the maximum dose of epinephrine is 0-2 mg or 200 pg, this equates to roughly 11 cartridges of I :100,000 epinephrine. 2. In a cardiac risk patient the maximum dose ofepinephrine is 0.04 mg or 40 pg, this equates roughly to two cartridges of l:000,000 epinephrine.

The tongue receives its blood supply from all of the following except Tonsillar branch ofthe facial artery Lingual artery Vertebral artery Ascending pharyngeal artery

Vertebral artery The lingual artery arises from the anterior surface ofthe external carotid artery, opposite the tip ofthe greater comu ofthe hyoid bone. It loops upward and then passes deep to the poste- rior border ofthe hyoglossus muscle to enter the submandibular region. The loop ofthe artery is crossed superficially by the hypoglossal nerve. Branches include dorsal lingual artery, suprahyoid artery and sublingual artery (t'hich supplies sublingual gland).lt terrninates as the deep lingual artery, which ascends between the genioglossus and inferior longitudinal muscles. Note: The floor ofthe mouth also receives its blood supply from the lingual artery Remember: . Motor innervation: from the hypoglossal nerve . /CNf,/,l). Sensory innervation: lingual (branch o-f trigeminal CN V-3) supplies the anterior two- thirds. glossopharyngeal (CN1X) supplies the posterior one-third (including vallate papillae), vagus epiglottis. /CN X) through the internal laryngeal nerve supplies the area near the r-ote: Besides the posterior l/3 of the tongue the glossopharyngeal nerve also supplies sensory innervation to the tonsil, nasopharynx and pharynx areas. . Taste: facial (CN VII) via chorda tympani supplies the antedor two-thirds; glossopha- ryngeal (CN L& supplies the posterior one-third. Note: The v€rtebral arteries arise from the subclavian arteries andjoin to form the basilar artery. The basilar artery is the main blood supply to the brainstem and connects to the Circle of Willis.

The ideal time to remove impacted third molaars are When the root is fully formed When the root is approximately two-thirds formed Makes no difference how much ofthe root is formed When the root is approximately one-third formed

When the root is approximately two-thirds formed Patient would be around the age of 17-21. At this time, the bone is more flexible and the roots are not formed well enough to havc de- veloped curves and rarely fracture during extraction. When the root is fully formed, the possibility increases for abnormal root morphology and for fracturc ofthe root tips during extraction. l. Patients who arc young tolerate surgery very well. Postoperative complications are usually ninimal. 2. Older individuals have the most postoperative difficulties, The bone is more dense and usually the patient responds more slowly to the entirc process (anesthesia and surgery).

When would you place a suture over a single extraction socket Routinely Never If the patient requests it When there is severe bleeding from the gingiva or ifthe gingival cuffis torn or loose

When there is severe bleeding from the gingiva or ifthe gingival cuffis torn or loose Normal post-€xtraction procedure: . -{li loose bone spicules and portions ofthe tooth, restoration, or calculus are removed from the socket as well as from the buccal and lingual gutters and the tongue . The socket must be compressed by the fingers to reestablish the normal width present before the buccal plate was surgically expanded. Note: The natural recontouring of the residual ridge occurs primarily by resorption ofthe labial-buccal cortical bone. . . Sutures are usually not placed unless the papillae have been excised The socket is covered with a gauze sponge that has been folded and moistened slightly at its center with cold water . The patient is insfucted to bite down on the pressure dressing for 30-60 minutes . -{ printed instruction sheet is given to the patient . .A. prescription for pain is given ifthe need is anticipated lf bleeding persists for some time following an extraction, it may be helpful to instruct the patient to bite on a tea bag. The tannic acid in the tea bag will help promote hemo- stasis. Alveolr p1ocffs and maxillary Can be avoided by innially creating an adequately sized incisiot caused by too much forc€; treated witlr pressure to stop bleeding and left Manqed wilh a figure-eighl sulure over the socket, sinus pr€cautions, artibiotics. and a nasal spny to preve.l inlection and keep the osliuft Most common complication; r€moved with elevators /i.e., srfaiarr, cryer, sro!, and rool tip picks. Fracture of teelh or reslorations For exampl€, maxillary molar rool into the maxillary sinus From too much force used to r€move teelh May occur in the area of lh€ .oots of lhe mandibular third molars. Lingual newe trav€ls very close to the lingual cortex of lhe mandible in this area- Can occur in 3% ofnandibular third molar extractions. Willh€al wilh irrigalion and localtreahent forpain control Remember: The most common cause ofpost-extraction bleeding is the failure ofthe pa- tient to follow post-extraction instructions.

When a max 3rd molar is displaced into the infratemporal fossa its usually displaced through the periosteum and located ? to the lateral pterygoid plate and ? to lateral pterygoid muscle with displacement medial, inferior medial, superior lateral, inferior lateral, superior

lateral, inferior The infratemporal fossa is an irregular space behind the maxilla. Its roof is formed by the greater wing ofthe sphenoid. The lateral pterygoid plate ofthe sphenoid is medial. La! erally, it is limited by the coronoid process and ramus ofthe mandible. The infratempo- ral fossa communicates with the pterygopalatine fossa through the pterygomaxillary fissure which is a cleft between the lateral pterygoid plate and the ma,rilla. It communi- cates with the orbit through the inferior ort ital fissure which is between the maxilla and the greater wing ofthe sphenoid. The pterygopalatine fossa is a small space behind and below the orbital cavity. It lies between the pterygoid plates ofthe sphenoid and palatine bone below the apex ofthe orbit. Clinical: Ifthere is good access and adequate light, a single cautious effort to retrieve the tooth with a hemostai can be made. Ifthe effort is unsuccessful, or ifthe tooth is not vi- sualized, the incision should be closed, the patient should be infonned, and prophylactic antibiotics should be prescribed. A secondary surgical procedure is performed 4-6 weeks later after lateral and posteroanterior radiographs are taken to locate the tooth in all three planes. After adequate anesthesia, a long needle is used to locate the tooth. Careful dis- section is performed along the needle until the tooth is visualized and subsequently remoyed. Note: Ifno functional problems exist after displacement, the patient may elect not to have the tooth removed. Proper documentation of this is critical.

Barbiturates are ? which results in a ? onset of action not lipid soluble, rapid slightly lipid soluble, delayed moderately lipid soluble, delayed very lipid soluble, rapid

very lipid soluble, rapid Barbiturates exhibit a dose-dependent CNS depression with hypnosis and amnesia. They are very lipid soluble, which results in a rapid onset of action. They are used most often for in- duction ofanesthesia because they produce unconsciousness in less than 30 seconds. Barbiturates: . Ultra-short acting: Methohexital (Brevital), thioper/''al (Pentothal), and thiamylal (Srir! tal) . Short and intermediate acting: Amobarbrtal (Amytal), pentobarbital (Nembutql), barbital . (Seconal), and Butabarbital fI'ioticet, Fiorinal) Long acting: Phenobarbital (LtminaQ Most commonly used barbiturates for induction of an€sth€sia: . Thiopental (Pentothal): Usually prepared as a 2.5To solution. An induction dose of 3-5 mg&g produces a loss ofconsciousness within 30 seconds and recovery in 5-10 minutes. Because the elimination half-life is 6-12 hor.rrs, patients may experience a slow recovery. When injected intravenously, it can be initating. Usually prepared as 2.5olo solution. pH is 1 0.5. . llethohexital /Brcvitdr: is somewhat less lipid soluble and less ionized at physiologic pH than thiopental. An induction dose of l-2 mg,&g produces loss ofconsciousness in less than 20 seconds and recovery in 4-5 minutes. The elimination half-life ofmethohexital is 3 hours, rrhich ailows a clearance rate that is 3 to 4 times faster than that ofthiopental. pH is 10.5. The side effect most often seen is hiccoughs. This is believed to be caused by rapid injec- tion of the Brevital. \ot.! . l. The most eff€ctive ag€nt in the initial treatment of respiratory d€pression due to the over dose ofbarbiturates is oxygen under positiv€ pressure. 2. A primary advantage of IV sedation is the ability to titrat€ individualized dosage.