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Oral Medicine Study Guide for Midterm – 2024.pdf

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Oral Medicine Study Guide for Midterm – 2024 The midterm exam will be given via ExamSoft in room 125. There are 74 multiple choice questions totaling (TBD) points with a 2.5 hour time limit (Questions are worth 1, 2 or 3 points each and are labeled such)....

Oral Medicine Study Guide for Midterm – 2024 The midterm exam will be given via ExamSoft in room 125. There are 74 multiple choice questions totaling (TBD) points with a 2.5 hour time limit (Questions are worth 1, 2 or 3 points each and are labeled such). There are 28 questions are based on 4 patient cases: Case 1: Patient with hx of ischemic CAD and HTN in need of an emergency tooth extraction. Case 2: Patient with hx of an arrhythmia, HTN and valvular heart disease taking an oral anticoagulant. Case 3: Patient with hx of ischemic CAD, arrhythmia, CHF, cardiomyopathy, HTN taking an oral anticoagulant. Case 4: Patient with hx of an autoimmune disease (SLE and/or RA and/or SS) taking an oral anticoagulant. Last pages of document has more info on these questions ↑↑ Bleeding / Hemostasis (including lab tests, Hemophilia A, [type I] von Willebrand's disease, and management of dental patients taking warfarin, a DOA or antiplatelet drugs): 9 questions Medical Risk Assessment for dental treatment (including Dentally-Modified ASA classification): 7 questions Antibiotic prophylaxis for prevention of BE and metastatic infections: 5 questions Recognition and Management of Medical Emergencies: 3 questions Autoimmune Disease (SLE, RA, SS): 4 questions Questions based directly on specific concepts presented in patient cases: 1 question Cardiovascular Disease (including hypertension, CHF, cardiomyopathy, angina pectoris, myocardial infarction, valvular [mitral, aortic] heart disease, infective endocarditis, vascular [cerebral, aortic] aneurysms and cardiac arrhythmias); /TIA: 12 questions. The Medical History Interview: 3 questions Integrated topic questions: 2 questions You MUST know: 1. The definition, purpose (use and/or misuse) of open-ended questions, closed-ended questions, contradiction questions, indirect questions, loaded questions, suggestive questions, and leading (or biased) questions during the medical history interview of a patient. a. Open-ended questions i. These prompt the patient into a narrative, which is an effective method of covering a complicated topic ii. Allow pt to respond fully without interruption 1. Example: “Can you tell me about your surgery that was performed last year?” a. Directs the patient to describe the entire topic with the expectation that most of the information will be contributory iii. Use: Open-ended questions are most effective with patients who are aware of health issues and can anticipate the information that is contributory. Open-ended questions can also calm anxious patients by providing an opportunity to talk their way through what may be an uncomfortable situation. iv. Don't use: This approach is less likely to be productive with unresponsive patients and individuals who digress from the topic. b. Closed-ended questions i. Demands specific information ii. Most specific and effective method of requesting information 1. Example: “When did you last see your physician?” a. Limits the pts. Response to a single sentence or less. c. Contradiction questions i. States inconsistent information and allows the pt to resolve the contradiction as with this example 1. Example: “Since you said that you do not have epilepsy, is there another reason for you to be taking a medicine that is usually prescribed to control seizures?” ii. Forces the pt to face the contradiction either by making another misleading statement or telling the truth. d. Indirect questions i. Presents a topic in such a way that the pt will reveal information beyond what is specifically requested by the question. 1. Example: “Have you had any complications during or after previous dental tx?” 2. Example is not designed to clarify such complications, but rather provide insight into the pts general attitude toward dental care. e. Loaded questions i. A specific type of indirect approach in which an emotional element is inserted into the phrasing to get the pts attention 1. Example: “Since it appears you have no interest whatsoever in taking care of your teeth, do you think that it might be best if I were to extract all of your teeth?” ii. Non verbal responses are often as revealing as the verbal response. f. Question types to AVOID: i. Suggestive questions 1. Provides the answer to the question a. Suggestive Example: “do you feel the pain in your left arm when you get it in your chest?” b. Better example: “when you get the pain in your chest, do you notice it anywhere else?” ii. Leading (biased) questions 1. Carries a suggestions of the kind of response for which the interviewer is looking. Suggests the answer within the question a. Example: “You haven’t used any recreational drugs, have you?” b. Better example: “Do you use recreational drugs?” 2. The appropriate content (i.e., what information belongs in) the following sections of a patient’s medical history: Source and Reliability, Biographic Information, Chief Complaint, History of the Present Illness (or History of the Chief Complaint), Pain Assessment, General State of Health, Past Medical History, Hospitalizations and Surgery, Current Medications, Current Medical Problems / Review of Systems, Allergies, Psychosocial History, Health Maintenance, Occupational and Environmental History, Diet, Sleep Patterns and Family History. a. Source and Reliability: Identifying data (age, gender), source of the history (usually the patient), and assessment of the patient's reliability to provide accurate information. b. Biographic Information: Date and place of birth, sex, race, ethnic background, and gender identity. c. Chief Complaint: A brief statement from the patient explaining the reason for seeking medical attention, ideally quoted in the patient's own words. d. History of the Present Illness: Details about recent changes in health related to the chief complaint, answering questions of what, when, how, where, which, who, and why. e. Pain Assessment: Evaluation of the patient's pain, including its location, intensity, duration, and any factors that alleviate or exacerbate it. f. General State of Health: Patient's overall health perception, including any recent physical examinations and current medical care. g. Past Medical History: Record of childhood and adult illnesses, including significant medical conditions and treatments. h. Hospitalizations and Surgery: Details of all hospital admissions and surgical procedures, including dates, reasons, and names of healthcare providers involved. i. Current Medications: List of all medications the patient is currently taking, including prescriptions and over-the-counter drugs. j. Current Medical Problems / Review of Systems: Evaluation of current medical issues organized by major organ systems, including pertinent positive and negative symptoms. k. Allergies: Description of all known allergies, including environmental, food, and drug-related reactions, along with specific symptoms experienced. l. Psychosocial History: Information on the patient's lifestyle, education, relationships, and any relevant social factors affecting health. m. Health Maintenance: Information on preventive care measures, such as vaccinations and screenings. n. Occupational and Environmental History: Details about the patient's work history, exposure to hazardous substances, and environmental factors affecting health. o. Diet: Overview of the patient's dietary habits and nutritional intake. p. Sleep Patterns: Information on the patient's sleep quality, duration, and any sleep disorders. q. Family History: Health information about immediate family members, including hereditary conditions and diseases that may affect the patient 3. The CCS classification system for angina pectoris, what it is used for; and how to assess a patient and classify them using this system. a. CCS is used to categorize the functional severity of a patient with Angina pectoris b. Divided into 4 Classifications based on the ability to perform metabolic events (METs) i. Class I (Ex tolerance: 7-8 METs) — ordinary physical activity doesn’t cause symptoms, only experience symptoms with strenuous physical activity [eg prolonged exercise] ii. Class II (Ex tolerance: 5-6 METs) — Slight limitation of ordinary activity—walking more than 2 blocks on level ground and climbing more than 1 flight of stairs without symptoms iii. Class III (Ex tolerance: 3-4 METs) — Marked limitation of normal physical activity. Angina occurs when walking 1-2 blocks at normal level and/or climbing 1 flight of stairs—shower/dress/make bed/play golf = no symptoms *Know what a person who is NOT capable of 4 METs can/can’t do without cardiovascular symptoms. iv. Class IV (Exercise tolerance: 1-2 METs) — Inability to perform any physical activity without discomfort; anginal symptoms may be present at rest 4. The NYHA (New York Heart Association) classification system for congestive heart failure, what it is used for; and how to assess a patient and classify them using this system. a. Congestive Heart Failure (CHF) — is a chronic progressive condition that affects the pumping power of your heart muscles. Ischemic symptoms are the result of oxygen deprivation secondary to reduced blood flow to a portion of the myocardium b. Class I — Asymptomatic — Patients with cardiac disease but without resulting in limitation or physical activity c. Class II — Symptomatic with moderate exertion — not symptomatic @ rest; ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain d. Class III — Symptomatic with minimal exertion e. Class IV — Symptomatic @ rest 5. The appropriate uses of the PT/INR, aPTT, BT, CT (via PFA-100), platelet count, and specific factor assays (i.e., what can each test be used for or detect). 1. Prothrombin Time (PT) / International Normalized Ratio (INR): Purpose: PT measures the time it takes for blood to clot by evaluating the extrinsic and common pathways of the coagulation cascade. Detection: ○ Prolonged PT/INR can indicate deficiencies in clotting factors (Factors I, II, V, VII, and X). ○ Used to monitor patients on warfarin (Coumadin) therapy to ensure appropriate anticoagulation. ○ Helps assess liver function as the liver synthesizes many coagulation factors. ○ Detects conditions such as Vitamin K deficiency and disseminated intravascular coagulation (DIC). ○ May be used to evaluate unexplained bleeding or bruising. 2. Activated Partial Thromboplastin Time (aPTT): Purpose: aPTT measures the time it takes for blood to clot, focusing on the intrinsic and common pathways of the coagulation cascade. Detection: ○ Prolonged aPTT can indicate deficiencies or inhibitors of clotting factors (Factors VIII, IX, XI, XII) and the common pathway factors (Factors I, II, V, X). ○ Monitors heparin therapy to ensure effective anticoagulation. This test does not work for Low Molecular Weight Heparin (LMWH) This test only works for unfractionated heparin ○ Detects hemophilia A (Factor VIII deficiency) and hemophilia B (Factor IX deficiency). ○ Identifies the presence of lupus anticoagulant or other specific inhibitors. ○ Useful in diagnosing conditions like DIC or severe liver disease. 3. Bleeding Time (BT): Purpose: BT is a historical test that evaluates primary hemostasis (the function of platelets and the blood vessel wall) and assesses the ability of small blood vessels to constrict and platelets to form a clot. Preoperative BT does NOT correlate with postoperative bleeding. Detection: ○ Prolonged BT may indicate platelet function disorders (e.g., von Willebrand disease) or qualitative platelet disorders. ○ Drugs causing prolonged BT = salicylates (aspirin), Non-COX-selective NSAIDS, platelet P2Y12 receptor inhibitors ○ Used to screen for inherited platelet function disorders and acquired conditions (e.g., uremia, aspirin use). ○ Rarely used in modern clinical practice due to its invasive nature and the advent of more specific tests. 4. Closure Time (CT) via PFA-100: Purpose: The PFA-100 test simulates the function of platelets under high shear stress, similar to that of a bleeding time test, but is more reproducible and sensitive. Collagen-adenosine diphosphate or Collagen-epinephrine coated Detection: ○ Evaluates platelet adhesion and aggregation (primary hemostasis). ○ Prolonged CT can indicate platelet dysfunction, von Willebrand disease, or the effects of antiplatelet medications (e.g., aspirin or clopidogrel). (aspirin-induced dysfunction = CADP CT: Normal, CEPI CT: Prolonged) ○ Useful in assessing platelet function in patients with a suspected bleeding disorder. Can NOT indicate a specific diagnosis. ○ May be used in the preoperative evaluation to predict bleeding risk. 5. Platelet Count: Purpose: Measures the number of platelets in a given volume of blood, providing an indication of the body’s ability to form clots. Detection: ○ Low platelet count (thrombocytopenia) can indicate conditions such as bone marrow disorders, leukemia, autoimmune diseases (e.g., ITP), and DIC. ○ High platelet count (thrombocytosis) can be associated with myeloproliferative disorders, chronic inflammation, or acute blood loss. ○ Important for evaluating the risk of bleeding, particularly before surgical procedures. 6. Specific Factor Assays: Purpose: Measure the activity or concentration of specific clotting factors in the blood to identify deficiencies or abnormalities. Detection: ○ Identifies specific clotting factor deficiencies (e.g., Factor VIII in hemophilia A, Factor IX in hemophilia B). ○ Useful in diagnosing inherited bleeding disorders and guiding specific replacement therapy. ○ Can be used to detect the presence of inhibitors (e.g., antibodies against Factor VIII). ○ Helps monitor the effectiveness of factor replacement therapy in patients with hemophilia. ○ Factor assays are vital in distinguishing between different causes of abnormal PT or aPTT results. 6. How to interpret INR and platelet count* results in relation to assessing for bleeding risk and adequate hemostasis for a patient that will require invasive or surgical dental treatment. * See required reading article: “Platelet count and platelet transfusion for invasive dental procedures in thrombocytopenic patients: A systematic review.” (Week 6) a. Due to the variations of responsiveness of the thromboplastin-to-anticoagulant effects in different laboratories performing PT test, the international normalized ratio (INR) was introduced to provide a means for standardization of PT results among laboratories b. The INR expresses PT (Prothrombin Time aka how fast your blood clots) results as a ratio of the patient's PT value divided by a control plasma PT value, which is then multiplied by the International Sensitivity Index (ISI) of thromboplastin. c. A “normal” INR value would be 0.9 – 1.2. However In our DMD-student dental clinics, routine, invasive dental treatment and simple oral surgery procedures may proceed if the patient's INR is 2.5 or less d. When the INR is higher than the recommended range, it means that your blood clots more slowly than desired, and a lower INR means your blood clots more quickly than desired e. PT is most sensitive to deficiencies in the vitamin K-dependent clotting factors II (prothrombin), VII, and X, also V f. PT [Prothrombin Time] is most frequently used to measure the effect and status of oral anticoagulation therapy with warfarin g. INR is the preferred method of reporting PT results because it standardizes results among labs h. INR test must be taken 48 hours or less before the invasive procedure. i. CoaguChek is the device for measuring INR i. allows pt to self monitor their INR, only need 1 drop of blood from a finger prick and 1 min to get INR result ii. j. DMD student is responsible to make sure the consultation with pt’s Dr is done and INR is good for the procedure. k. At ULSD for DMD level treatment: patient must have INR 90% cases), viral, fungal c. Most commonly develops on mitral valve, aortic valve, both mitral + aortic tricuspid, rarely the pulmonic valve d. DO NOT NEED PROPHYLAXIS → Including: Implantable cardiac pacemakers or defibrillator, implantable vagus, spinal, or dorsal column stimulators, intra-aortic balloon pumps, arterial stents or grafts, prosthetic vascular patches/conduits, cardiac stents or peripheral vascular stents, cerebrospinal fluid shunts, inferior vena cava filter (greenfield filter), AV shunts, subq implantable drug delivery pumps, breast, penile, intraocular lens implants...etc. e. Evidence for hematogenous infections in such patients with oral microorganisms is extremely limited or non-existent f. Equally, there is no evidence that AB prophylaxis is effective in prevention of infections in these patients g. AB prophylaxis is not routinely recommended for patients who undergo dental or other invasive procedures h. If the attending physician requests AB prophylaxis for such patients before dental treatment…the dentist can state that there is no medical reason for such practice and request that the physician provide the prophylaxis. i. So when does a pt. Need antibiotic prophylaxis? → → just remember the don’ts per the panopto Antibiotic prophylaxis is recommended for patients with the highest risk of adverse outcome from infective endocarditis, including those with: Prosthetic cardiac valves History of infective endocarditis Surgical or transcather pulmonary artery valve or conduit placement such as Melody valve and Contegra conduit History of cardiac valve repair with prosthetic devices LVAD or implantable heart Cardiac transplantation recipients who develop cardiac valvulopathy (donor heart that has a pathology) unrepaired cyanotic congenital heart disease (TOF, TGA) Completely repaired congenital heart defect with prosthetic material/device (whether placed by surgery or catheter), during the first 6 months after the procedure Repaired CHD with residual hemodynamic defect at sit or adjacent to the site of a prosthetic device or patch Certain congenital heart diseases i. For these high-risk patients, prophylaxis is recommended for dental procedures involving manipulation of gingival tissue, periapical region of teeth, or perforation of oral mucosa. j. He said know the adult doses of the this chart in the panopto i. He said you don’t need to know IV doses/meds for this exam but we will for clinical pharm ii. 1. Note: Clindamycin is no longer recommended. Regular dental care and good oral hygiene are essential to reduce the risk of infective endocarditis. 2. If a series (multiple appts) of invasive (bacteremic) dental procedures is required, it is suggested: a. either an alternative antibiotic regimen (i.e., an antibiotic from a different pharmacologic class) should be used each time b. OR there should be an interval of at least 4 weeks between [elective] procedures to both reduce the potential for the emergence of resistant organisms and allow repopulation of the mouth with antibiotic susceptible flora. 3. If a patient is already receiving oral antibiotic therapy for several days or longer with an antibiotic that is also recommended for IE prophylaxis for a dental procedure: a. If delaying dental treatment is not an option, then it is prudent to select an antibiotic from a different pharmacologic class rather than to increase the dosage of the current antibiotic. k. The above medical devices ↑↑ DO NOT NEED antibiotic prophylaxis for dental procedures l. When antibiotics are used, six events may occur with only one being beneficial: 1. The antibiotic aids the host defenses to gain control and eliminate the infection. ii. The antibiotic may also: 1. precipitate an adverse reaction: a. allergic reactions (e.g., anaphylaxis) b. toxic reactions or other adverse reactions 2. initiate a superinfection with resistant bacteria 3. promote microbial chromosomal mutations to resistance 4. encourage resistance gene transfer to susceptible species 5. promote the expression of dormant resistance genes 15. The etiology of hemophilia A and how to assess bleeding risk, manage bleeding and improve hemostasis in a dental patient with hemophilia A that will require invasive or surgical dental treatment. (see PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) a. Congenital bleeding disorder b. Deficiency in functional Plasma clotting factor VIII (F-VIII) → excessive bleeding c. X-linked recessive d. “Most common of the inherited coagulation bleeding disorders” e. 1 in 5000 male births, more than 20,000 individuals in US have hemophilia A f. F-VIII assays used to classify severity of the disease: 1. Normal F-VIII levels: ○ Normal levels of Factor VIII in the blood are between 50 and 150 U/dL. This is what a person without hemophilia would typically have, meaning their blood clots normally. 2. Mild Hemophilia A: ○ When the Factor VIII levels are between 6% and 50% (or 5-20 U/dL), the condition is considered mild. People with mild hemophilia may not have frequent bleeding issues, but they can experience bleeding after surgeries, dental work, or significant injuries. 3. Moderate Hemophilia A: ○ With Factor VIII levels between 1% and 5% (or 2-5 U/dL), the condition is moderate. Individuals with moderate hemophilia may experience bleeding episodes after minor injuries and might also have occasional spontaneous bleeding episodes (bleeding without an obvious cause). 4. Severe Hemophilia A: ○ When Factor VIII levels are ≤ 1% (or less than 2 U/dL), the condition is classified as severe. People with severe hemophilia have frequent spontaneous bleeding episodes, often affecting joints and muscles, and they are at high risk of life-threatening bleeds (e.g., internal bleeding or brain bleeds) without treatment. g. Factor VIII concentrate (Humate-P) i. Control spontaneous and traumatic hemorrhage in patients with hemophilia A ii. The new recombinant factor VIII is stable w/o added human serum albumin (decreased risk of disease transmission like HIV) h. Dose calculators for factor VIII replacement are directed toward achieving FVIII activity level of: i. 20-50% for most mild hemorrhages: gingival bleeding, simple oral surgery ii. At least 50% for severe bleeds (ie trauma), or prophylaxis prior to major dental oral surgery or general surgery iii. 80-100% in life threatening hemorrhage i. Alloantibodies (Inhibitors) and Factor VIII Treatment Alloantibodies: In some patients with severe Hemophilia A, after exposure to Factor VIII (F-VIII) concentrates, the body can develop inhibitors (alloantibodies) that neutralize the clotting function of F-VIII. This happens in 30% of severe Hemophilia A patients, making standard F-VIII replacement therapy ineffective. Bypassing Agents: In these cases, bypassing agents like recombinant activated Factor VII (rFVIIa, NovoSeven RT) or anti-inhibitor coagulant complex (AICC) are used. These agents work around the need for F-VIII to control bleeding. ○ rFVIIa (NovoSeven RT): This is often the first choice in 75% of patients with inhibitors and is used for stopping spontaneous bleeding and preventing excessive bleeding during surgeries. ○ Dosage: The recommended dose is 70-90 mcg/kg, given immediately before surgery, and repeated every 2-3 hours during surgery until hemostasis (blood clotting) is achieved. Desmopressin (DDAVP) for Mild Hemophilia A For mild F-VIII deficiency, patients can often be managed in a dental office for less invasive procedures (scaling, soft tissue surgery, simple extractions) without the need for F-VIII replacement. Desmopressin (DDAVP): This medication helps by stimulating the release of stored F-VIII from endothelial cells, temporarily increasing plasma F-VIII levels. It’s useful for preparing patients for dental or minor surgical procedures. ○ IV Dosage: 0.3 mcg in 100 mL saline, infused over 30 minutes. ○ Nasal Spray: 150 mcg per nostril, with the peak effect 60-90 minutes after administration. ** Said in lecture know how to use the spray ** ○ A test dose of DDAVP should be done before the procedure to ensure an appropriate rise in F-VIII levels. There should be at least 1 week between test dose and procedure to allow replenishment of the body's F-VIII stores. ○ e-aminocaproic acid (EACA, Amicar) or Tranexamic Acid: These can be combined with DDAVP for patients with mild Hemophilia A, as they help stabilize blood clots. Factor VIII Replacement for Moderate to Severe Deficiency For patients with moderate to severe F-VIII deficiency without inhibitors, F-VIII replacement is necessary before invasive dental procedures like extractions or mucosal surgeries. Humate P: A single dose is given to reach a peak F-VIII level of 20-50%, along with a dose of 20 mg EACA to help prevent excessive bleeding. Management for Severe Deficiency with Inhibitors Patients with moderate to severe F-VIII deficiency with inhibitors (alloantibodies) require recombinant activated Factor VII (rFVIIa, NovoSeven RT) before invasive dental procedures. This ensures bleeding is controlled when F-VIII is not effective due to inhibitors. j. How to assess bleeding risk i. Excessive bleeding after operation, surgery, extractions 1. What was the procedure, did bleeding start soon after surgery or delayed onset, length of time of prolonged bleeding, estimated amt of blood loss, what intervention was needed to manage bleeding, any procedures since the episode of excessive bleeding????? ii. Excessive bleeding after trauma iii. Occurrence of spontaneous bleeding iv. Use of any drugs that may cause bleeding v. Past and present illness associated with bleeding vi. Presence of bleeding problems in relatives vii. Have you ever had bruising with minimal/no trauma, especially if you could feel a lump under it? viii. Have you ever had prolonged bleeding from a trivial wound lasting more than 15 mins or recurring spontaneous bleeding 7 days post wound? ix. Spontaneous nose bleed? x. Bloody stool? xi. Heavy menses w/ clots >1 inch in diameter? 16. The etiology of von Willebrand’s disease and how to assess bleeding risk, manage bleeding and improve hemostasis in a dental patient with type I von Willebrand’s disease that will require invasive or surgical dental treatment. (see PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) a. The “most common of all inherited bleeding disorders” b. Affects 1-2% of US population c. Caused bv a deficient or defective von Willebrand factor - a multimeric protein that mediates platelet adhesion d. In lecture said we don’t need to know the types ↓↓ i. Type I vWD 1. Autosomal dominant 2. The most common form (75-85% cases) 3. Mild to moderate quantitative deficiency in vWF 20-50% of normal levels 4. Mild abnormal bleeding ii. Type II 1. Autosomal dominant 2. 20-25% of cases 3. 4 variants IIA, IIB, IIM, IIN based on characteristics of the dysfunctional vWF and is associated with mild to moderate bleeding iii. Type III 1. Autosomal recessive 2. Most rare form 3. Most severe form 4. Very little or no detectable plasma or platelet vWF resulting in profound bleeding disorder e. Diagnosis i. Initial tests suggestive of vWD in patient with history of abnormal/prolonged bleeding 1. ii. Confirmatory lab studies for vWD are directed toward documenting a deficiency of vWF 1. f. Dental management of patients with VW disease i. The mainstay of dental management of vWD is the replacement of the deficient vWF before performing dental procedures likely to result in bleeding ii. Desmopressin (DDAVP) - useful to release stored vWF from endothelial cells (HE SAID REALLY UNDERSTAND THIS DRUG IN LECTURE) 1. Effective for controlling bleeding from minor surgical procedures in most patients with mild type I vWD and some type II variants 2. DDAVP is not effective in type IIA and potentially dangerous in IIB (increased risk of bleeding and thrombocytopenia) 3. 0.3 mcg/kg in 100mL saline IV infused over 30 min (peak effect 30-60 min) 4. Nasal spray if patient is >50kg: 300mcg (one 150 spray each nostril) prior to dental tx (peak effect 60-90min)**** Know spray*** iii. Humate P (factor VIII concentrate) 1. Useful to correct bleeding abnormalities in type IIA, IIB, III vWD without alloantibodies (inhibitors) 2. vWF has a separate function of binding factor VIII coagulant protein and protecting it from degradation therefore a deficiency in vWF gives risk to a secondary decrease in factor VIII levels. a. This can mimic or exacerbate the bleeding problems seen in hemophilia A iv. e-aminocaproic acid (EACA, Amicar) - Dont need to know doses 1. 50-60 mg/kg every 4-6 hours → if pt is unresponsive to conventional methods v. Tranexamic acid- adjunctive - dont need to know doses 1. 20-25 mg/kg every 8-12 hours 2. Can be administered orally or IV as adjunct therapy concurrent with DDAVP or Humate P to improve hemostasis during oral surgery 17. The etiology, medical management/treatment, assessment, and dental management of patients with thrombocytopenia, (specifically ITP) that will require invasive or surgical dental treatment. (see PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6], as well as case studies in Week 6.) a. ITP (idiopathic thrombocytopenic purpura) increased platelet destruction or excessive pooling 1. AKA, immune thrombocytopenic purpura or immune thrombocytopenia (They now tend to use "immune" instead of "idiopathic" for ITP since we now know the destruction of platelets is an autoimmune-mediated event) ii. Low platelet count is associated with spontaneous bleeding, prolonged bleeding time, ecchymosis (bruise), petechiae iii. Symptoms of Patients with ITP: 1. Petechiae: small, pinpoint hemorrhages in the skin 2. Ecchymosis: bruising 3. Spontaneous bleeding iv. Platelet counts 1. 20,000-50,000/µL - petechiae and ecchymosis observed following mild trauma 2. 1cm) 3. Telangiectasias/spider angiomas 4. Jaundice/pallor/cyanosis 18. The major indications (uses for) anticoagulation therapy using warfarin and direct oral anticoagulants (DOCs), and the management and hemostasis concerns of dental patients taking warfarin or DOCs that will require invasive or surgical dental treatment. (see PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) a. Warfarin: Uses i. Prevention of stroke in patient with AFib ii. Prevention and treatment of Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) iii. Patients with high risk factors such as mechanical heart valves (DOAC’s are not used for mechanical heart valves) b. Dental Management of Patients taking Warfarin i. c. 5 DOACs have recently been approved for use in US and are increasingly being used as an alternative to Warfarin (they are more expensive than warfarin) i. Direct Reversible Thrombin Inhibitor (DTI) 1. dabigatran-Pradaxa a. Pronounced duh-bi-guh-Tran ii. Reversible factor Xa inhibitor - FXal (BEAR) 1. Betrixaban - Bevyxxa 2. Edoxaban - Savaysa 3. Apixaban - Eliquis 4. Rivaroxaban - Xarelto a. -abans are factor Xa inhibitors iii. These 5 DOACs cannot be used for mechanical valves iv. All have considerably shorter half life than warfarin v. People taking warfarin must go for regular PT/INR testing, while those taking a DOAC do not need to have PT/INR testing 1. Conventional coagulation tests (PT and PTT) have significant limitations when used to quantify DOACs, basically useless d. Clinical indications i. Decreased risk of stroke and systemic embolism in patients w/non-valvular a-fib ii. Treatment and prevention of DVT and pulmonary embolism e. Dental management of patients taking DOACs non-surgical - Continue usual DOAC dose regimen i. Low bleeding risk 1. Option 1 (for pts with high risk for thromboembolism) continue usual DOAC dose and use adjunctive local hemostatic measures 2. Option 2 (for pts with low risk for thromboembolism) have patient skip usual dose of DOAC 4-24 hours prior to procedure and use appropriate local hemostatic methods (ie sutures, absorbable gelatin sponges, fibrin glue, topical thrombin, local pressure) ii. High bleeding risk 1. Discontinue DOAC 24-48 hours before surgery or longer depending on: risk of bleeding based on type of procedure, presence/degree of impaired renal function, presence of other risks for impaired hemostasis 2. Use adjunctive local hemostatic methods as indicated (pressure, glue, etc) f. Patients with High Risk for Thromboembolism i. Recent DVT or pulmonary embolism (within 3 months) ii. Protein C or Protein S deficient iii. High-risk mechanical heart valves (he said something about the bi-leaflet valve not being a High risk valve) iv. High Risk atrial fibrillation with CHADsVAS score of 5 or higher 1. Slide 72 of Hemostasis notes say a score 5 or higher. Also said this in Lecture v. Atrial Fibrillation with Rheumatic Heart Disease vi. Recent stroke or TIA caused by atrial fibrillation or heart disease (CHF) within 6 months vii. Morbid obesity or immobility g. Patients with Impaired renal function-increases the ½ life of dabigatran, rivaroxaban, apixaban, edoxaban and betrixaban (ALL DOACs). i. Thus increases the risk of over anticoagulation and bleeding complications ii. Particularly important for dabigatran and endoxaban which are excreted in kidney to a greater extent than the others iii. Upon discontinuation of drug-will take longer for their anticoagulant effect to diminish with impaired renal function 19. The cardiovascular indications for the use of aspirin and antiplatelet drugs (e.g., clopidogrel), and the management and hemostasis concerns of dental patients taking aspirin and antiplatelet drugs (e.g., clopidogrel) that will require invasive or surgical dental treatment. (see PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) Platelet P2Y12 ADP Inhibitors: ○ Clopidogrel (Plavix), Prasurgrel (effient), Ticagrelor (brillanta) These drugs inhibit platelet aggregation by selectively inhibiting adenosine diphosphate (ADP) stimulation of P2Y12 receptor. Used as single agents or combined with aspirin (dual antiplatelet therapy) to prevent thrombotic cardiovascular or cerebrovascular events. Dual antiplatelet therapy is the primary prevention strategy against stent thrombosis after placement of drug-eluting metal stents in patients with coronary artery disease. All he said you need to know about the left slide is that they have a considerably shorter half life than warfarin. Don't need to know specific values These drugs have relatively short half live (6-9 hrs), but affect platelet function for a long time (3-10 days) Salicylates: ○ Aspirin (non-selective COX inhibitor) covalently acetylates to cyclooxygenase and blocking production of thromboxane A2 and inhibiting platelet aggregation. ASA (aspirin) is irreversible on platelets Patients who take a high dose for long term, a clinically significant effect on hemostasis may persist from 36 hours up to 7 days after last dose of ASA was administered. Reversal: no specific agents for both ASA and NSAIDs. ○ Other NSAIDS Generally do not lead to bleeding problem, and invasive dental procedures can be performed without discontinuing these ○ Low-dose ASA use alone, or combined with other antiplatelet drugs (e.g., clopidogrel, ticlopidine, prasugrel, ticagrelor) have minimal impact on the amount and duration of bleeding following routine dental treatment procedures, including uncomplicated multiple extractions, especially when appropriate adjunctive local hemostatic methods are used. ○ For patients receiving dual antiplatelet therapy and/or with chronic kidney disease, the risk of hemorrhage after tooth extraction is increased, and the use of adjunctive local hemostatic methods (i.e., at least sutures) are recommended.* Protease-activated receptor-1 (PAR-1) antagonist: ○ Vorapaxar (zontivity) Other Antiplatelet Drugs: ○ Dipyridamole, cilostazol, ticlopidine 20. The Dental Treatment Guidelines for Adult Patients Based on Presenting Blood Pressure (see “Table 7" in the OM notes on “Hypertension” [Week 3]). ***Know the ASA classification for hypertension well 21. What conditions place a patient at high-risk for a thromboembolic event according to the American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. (see slide #72 in PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) a. Factors Increasing the Risk of Thromboembolic Event i. Recent DVT or PE (within 3 months). ii. High-risk prothrombotic condition (e.g., protein C or protein S deficiency). iii. High-risk mechanical heart valves (i.e., all mechanical mitral valves, and aortic caged-ball or tilting disk types). iv. High-risk atrial fibrillation (i.e., CHA₂DS₂-VASc ≥ 5). v. Atrial fibrillation with rheumatic heart disease. vi. Recent stroke or TIA from atrial fibrillation or valvular heart disease (within 6 months). vii. Morbid obesity or immobility. 22. The indications for the use of the major categories of cardiovascular drugs presented and discussed in the case studies (e.g., cardiac glycosides, thiazide and loop diuretics, sodium channel blockers, aldosterone antagonists, angiotensin-II receptor blockers, beta-blockers, ACE inhibitors, potassium channel blockers, nitrates, antiplatelet drugs, etc.). Major Categories of Cardiovascular Drugs and Their Indications Cardiac Glycosides ○ Example: Digoxin ○ Indications: Heart failure (HFrEF), atrial fibrillation ○ Mechanism: Increases myocardial contractility and slows AV node conduction Thiazide Diuretics ○ Example: Hydrochlorothiazide ○ Indications: Hypertension, heart failure ○ Mechanism: Inhibits sodium reabsorption, reducing blood volume Loop Diuretics ○ Example: Furosemide ○ Indications: Heart failure, hypertension with fluid retention ○ Mechanism: Inhibits sodium, potassium, and chloride reabsorption in the loop of Henle Sodium Channel Blockers ○ Examples: Lidocaine, Flecainide ○ Indications: Ventricular and atrial arrhythmias ○ Mechanism: Stabilizes abnormal electrical activity by blocking sodium channels Aldosterone Antagonists ○ Example: Spironolactone ○ Indications: Heart failure, resistant hypertension ○ Mechanism: Blocks aldosterone, reducing sodium retention and blood pressure Angiotensin II Receptor Blockers (ARBs) ○ Example: Losartan ○ Indications: Hypertension, heart failure, diabetic nephropathy ○ Mechanism: Blocks angiotensin II, reducing vasoconstriction and aldosterone secretion Beta-Blockers ○ Examples: Metoprolol, Carvedilol ○ Indications: Hypertension, heart failure, arrhythmias, post-MI ○ Mechanism: Blocks beta-adrenergic receptors, reducing heart rate and contractility ACE Inhibitors ○ Example: Lisinopril ○ Indications: Hypertension, heart failure, post-MI, diabetic nephropathy ○ Mechanism: Inhibits ACE, reducing angiotensin II production and blood pressure Potassium Channel Blockers ○ Example: Amiodarone ○ Indications: Atrial and ventricular arrhythmias ○ Mechanism: Blocks potassium channels, prolonging repolarization Nitrates ○ Example: Nitroglycerin ○ Indications: Angina, acute heart failure ○ Mechanism: Dilates veins and coronary arteries, reducing myocardial oxygen demand Antiplatelet Drugs ○ Examples: Aspirin, Clopidogrel ○ Indications: Prevention of heart attacks, strokes, stent thrombosis ○ Mechanism: Inhibits platelet aggregation, reducing clot formation Comparison of commonly used blood thinners we talked about: ○ Warfarin: Long-term anticoagulation for conditions like atrial fibrillation, mechanical heart valves, DVT/PE. ○ Heparin: Short-term or acute anticoagulation in hospital settings, including DVT/PE treatment or bridging therapy. ○ Plavix: Antiplatelet drug used to prevent heart attack, stroke, or stent thrombosis in cardiovascular disease. ○ Aspirin: Antiplatelet drug used for preventing heart attacks and strokes, especially in patients with a history of cardiovascular disease or after stent placement. Often used in combination with Plavix for dual antiplatelet therapy. 23. What dental procedures are considered “non-surgical dental treatment with no significant bleeding”, “low-bleeding-risk surgical dental procedures” and “high-bleeding-risk surgical dental procedures”. (see slide #79 in PowerPoint: “Hemostasis and Bleeding Risk in the Dental Patient” [Week 6].) a. 24. The emergency management of a patient experiencing chest pain or vasodepressor syncope during dental treatment. (see “Medical Emergency Flowchart” and related lecture content.) Angina pectoris and acute myocardial infarction are the two most common cardiac causes of chest pain in dental settings. ○ If a patient experiences chest pain for the first time, the dentist should treat it as a potential acute myocardial infarction and immediately call for emergency medical services. For conscious patients with a patent airway: Seat the patient upright and provide reassurance until the pain subsides. Schedule a follow-up appointment and discharge the patient only when the pain has completely resolved. Instruct the patient to be accompanied by an adult. For known cases of angina pectoris: If the patient has a glyceryl trinitrate tablet or spray, advise them to chew or spray it under the tongue. Do not discharge the patient until the pain has completely resolved. Ensure the patient is accompanied by an adult. For unconscious patients: Establish a patent airway and initiate CPR until emergency medical services arrive. a. b. c. He said in lecture that if the patient is in a lot of pain (elephant sitting on chest, can barely breathe), then you should skip straight to calling 911 i. If patient has symptoms of nausea, sweating, and chest pain → call 911 immediately d. Rule of 3 → 3 nitros over 15 mins and no improvement → call 911 e. You can give a patient who is on warfarin, aspirin if they are having a heart attack f. If patient is on dual antiplatelet therapy (plavix combined with aspirin) → not imperative to have the pt take another 325mg of aspirin. 25. The initial signs and symptoms of a myocardial infarction and stroke. a. Clinical presentation of Myocardial Infarction i. Crushing substernal chest pain usually lasting longer than 30 minutes. ii. Pain is unrelieved by rest or sublingual nitroglycerin or is rapidly recurring iii. Pain radiates to the left or right arm, neck, jaw, back, shoulders, or abdomen and is not pleuritic in character iv. Pain may be associated with dyspnea, diaphoresis, nausea, or vomiting v. b. Clinical presentation of Stroke Sudden numbness or weakness: Typically on one side of the face, arm, or leg. Sudden confusion or trouble understanding speech: Difficulty speaking or understanding others. Sudden trouble seeing in one or both eyes: Vision changes, such as blurred or double vision. Sudden trouble walking, dizziness, or loss of balance or coordination: Difficulty walking or maintaining balance. Sudden severe headache with no known cause: A severe headache that comes on without a clear reason 26. The clinical presentation (including signs and symptoms), medical management and dental management of a patient with dilated cardiomyopathy. a. Definition: i. Dilated cardiomyopathy (DCM) is a condition where the heart's ability to pump blood is diminished due to an enlargement and weakening of the ventricles, the heart's main pumping chambers. b. Physical Findings and Clinical Presentation i. Increased jugular venous pressure (indicative of fluid overload) ii. Small pulse pressure (reflecting low stroke volume) iii. Pulmonary rales (crackling sounds in the lungs due to fluid), hepatomegaly (enlarged liver), peripheral edema (swelling in the legs and feet) iv. S3 and S4 heart sounds (associated with abnormal ventricular filling) v. Mitral regurgitation (backflow of blood through the mitral valve), tricuspid regurgitation (less common) c. Patients with any type of cardiomyopathy, including dilated, hypertrophic, or restrictive, are at risk for specific cardiovascular complications that must be evaluated and addressed before dental treatment. These complications include: i. Congestive heart failure (CHF): Patients with CHF may experience fluid buildup, shortness of breath, and fatigue, which can impact their ability to tolerate dental procedures. ii. Atrial and ventricular arrhythmias: These irregular heart rhythms can increase the risk of medical emergencies during treatment. iii. Cardiac valvular pathology: The most common valvular issue in DCM is mitral regurgitation (mitral insufficiency), though other valvular problems like tricuspid regurgitation may also occur. 1. Note on Prophylactic Antibiotics: a. Patients with cardiac valvular pathology (e.g., mitral insufficiency) do not generally require prophylactic antibiotics prior to dental treatment unless they have a history of infective endocarditis or other high-risk factors, in accordance with current guidelines. 27. The cardiovascular indications (conditions), dental treatment procedures and orally administered prophylactic antibiotic regimens currently recommended (the 2021 modification of the 2007 guidelines) by the American Heart Association for the prevention of bacterial endocarditis in adults. (Sample question format appears below.) a. AHA Guidelines for Bacterial Endocarditis Prevention (2021 Update) i. Cardiovascular Indications for Antibiotic Prophylaxis: 1. Prophylaxis is recommended for patients with: a. Prosthetic cardiac valves or material used for valve repair b. Previous infective endocarditis c. Certain congenital heart defects (CHD), either unrepaired or with residual defects after repair d. Cardiac transplant patients with abnormal valve function b. Dental Procedures Requiring Prophylaxis: i. Antibiotics are recommended for dental procedures involving: 1. Gingival tissue manipulation 2. Periapical region manipulation 3. Oral mucosa perforation c. 28. The clinical presentation (including signs and symptoms), medical management and dental management of patients with (abdominal) aortic aneurysms and cerebral vascular aneurysms. a. Abdominal Aortic Aneurysms i. Abdominal aortic artery is dilated (surgery is indicated when AAA is >5.5 cm) 1. Normal AAA size a. men - 2.3 cm b. women- 1.9 cm ii. Signs and symptoms 1. Pulsatile epigastric mass that may or may not be tender (can be asymptomatic*) 2. Abdominal pain radiating to the back, flank, and groin 3. Early satiety, nausea, and vomiting caused by compression of adjacent bowel 4. Venous thrombosis from iliocaval venous compression 5. Discoloration and pain of the feet with distal embolization of the thrombus within the aneurysm 6. Flank and groin pain from ureteral obstruction and hydronephrosis iii. Dental management of patients with aneurysms: 1. Patients with aneurysm could have complications with epinephrine, if the BP gets too high the aneurysm could burst. Take caution when injecting 2. If a local anesthetic containing a vasoconstrictor is used, it is advisable to follow the vasoconstrictor dose reduction guidelines 3. It might be smart to use a LA without a VC when treating a patient with an aneurysm, this is depending on the procedure a. (small procedure, no VC). b. If doing large procedure, follow dose reduction guide to 2 carpules VC. iv. Medical Tx 1. Surgery to treat an aneurysm will not be done until it reaches 5.5 cm or larger. The risk of fixing the aneurysm does not outweigh the benefits until it reaches this size. b. Cerebral Vascular Aneurysms Clinical Presentation: Often asymptomatic until rupture (may cause focal neurologic deficit) Ruptured aneurysm presents as sudden severe headache, neck stiffness, altered consciousness Unruptured aneurysms may cause headaches, visual disturbances, or cranial nerve palsies Medical Management: Surgical clipping or endovascular coiling for ruptured aneurysms Treatment of unruptured aneurysms based on size, location, and patient factors Blood pressure control and smoking cessation to reduce rupture risk Dental Considerations: Assess bleeding risk if on antiplatelet/anticoagulant therapy Avoid extreme positional changes Consider shorter appointments to reduce stress Use caution with vasoconstrictors in local anesthetics 29. The clinical presentation (including signs and symptoms), pharmacologic and nonpharmacologic (surgical) medical management/treatment (as applicable), dental treatment risk assessment and dental management (treatment modifications) of patients with: a. a history of previous stroke and/or TIA i. Transient Ischemic Attack (TIA) = transient neurologic dysfunction caused by focal brain or retinal ischemia 1. Clinical presentation (signs/symptoms) = can last from 1-24 hours max, patient will recover fully a. Ipsilateral monocular visual disturbances b. Contralateral motor or sensory dysfunction c. Language dysfunction d. Vertigo, diplopia, dysphagia 2. Pharmacologic Tx a. First line treatment = Aspirin b. clopidogrel (Plavix) 3. Non-pharm Tx a. If carotid artery TIA = surgery or stent placed in patients not candidates for surgery b. Carotid Endarterectomy (a surgical procedure that removes plaque buildup from an artery to improve blood flow and reduce the risk of stroke or other complications) c. Smoking cessation, HTN control, lower cholesterol ii. Stroke ( - Cerebrovascular Accident) = acute brain injury caused by decrease in blood (thrombosis/embolism) or hemorrhage 1. Clinical Presentation (signs/symptoms) = 70-80% are caused by thrombosis or embolism a. Motor, sensory, or cognitive deficits, or a combination, depending on the distribution and extent of involved vascular arteries b. More common manifestations include contralateral motor weakness or sensory loss, as well as language difficulties (aphasia; predominantly left-sided lesions) and visuospatial neglect phenomena (predominantly right-sided lesions). 2. Pharmacologic Tx a. 3-6 hours after stroke = injection of clot busting agents - TPA (tissue plasminogen activator) i. Antiplatelet therapy = Aspirin, Clopidogrel (plavix), Ticlopidine b. Cardioembolic stroke = Warfarin, DOAC c. Heparin = if pt also has A. Fib 3. Non-Pharm Tx = surgery a. Don’t lower BP too quickly after stroke b. Smoking cessation, control BP, exercise, diet (prevention) c. Carotid Endarterectomy iii. Dental Management 1. Atherosclerotic lesions at the carotid bifurcation frequently are calcified and have been shown to be detectable on the panoramic dental radiographs of neurologically asymptomatic patients. Identifying a calcified carotid artery atheroma on a panoramic radiograph is of major clinical importance. Patients with such calcifications may be at a significantly increased risk of experiencing , and should be referred to an appropriate physician for confirmation of the findings and determination of the extent of disease. a. The ULSD Radiology Division has a specialized referral/consultation form to send to the physician of a patient that demonstrates radiographic evidence of a calcified carotid artery atheroma. 2. These patients could be taking anticoagulant drugs that could lead to excessive bleeding 3. Loss of sensory stimuli in oral cavity may occur = diminished gag reflex 4. Use of Vasoconstrictor is NOT contraindicated, but should still be used with caution b. Hypertension i. Primary HTN (90% of pts) has no one defined cause = Usually asymptomatic ii. Secondary HTN (10% of pts) occurs secondary to some specific, identifiable etiology 1. renal disease, endocrine disorders, neurogenic disorders, pheochromocytoma, coarctation of aorta → fix the etiology the HTN will resolve iii. Pharmacologic Tx 1. ACE Inhibitors = Lisinopril 2. ARB (Angiotensin II Receptor blocker) = Benicar (Olmesartartan), Losartan 3. Beta Blockers = Metoprolol, Propranolol, Carvedilol 4. Diuretics = hydrochlorothiazide (thiazide diuretic), furosemide (loop diuretic), chlorothiazide 5. Aldosterone Antagonist = Eplerenone 6. Calcium Channel Blockers = Amlodipine a. CHF: ACE inhibitors, ARBs, beta blockers, diuretics, aldosterone antagonists b. Post-MI: beta blockers, ACE inhibitors, aldosterone antagonists c. High cardiovascular risk: beta blockers, ACE inhibitors, calcium channel blockers, diuretics d. Diabetes: ACE inhibitors, ARBs, calcium channel blockers, beta blockers, diuretics e. Chronic kidney disease: ACE inhibitors, ARBs f. Recurrent stroke prevention: ACE inhibitors, diuretics i. Two-drug combination is necessary for most patients with stage 2 hypertension. Combination of a diuretic with another agent is preferred unless there are compelling indications to use other agents. g. i. The table above only applies to pts. before they start taking blood pressure medications. Also this classification requires an average of two or more seated blood pressure readings taken on each of two or more office visits. (can’t be from one reading) ii. Hypertensive crisis → 180/120 iii. Hypertensive emergency - severe elevation in BP because of impending organ dysfunction. iv. Hypertensive Urgency - severe elevation in BP without end-organ damage iv. Non-Pharm Tx 1. Lifestyle changes = lose weight, limit alcohol, reduce sodium, stop smoking v. Dental Management 1. For patients with controlled hypertension, follow the dose reduction guidelines for the use of local anesthetic containing a vasoconstrictor, especially if taking non-selective b-blocker a. Local anesthetics containing a vasoconstrictor are usually not recommended for use in patients with uncontrolled or poorly controlled (ASA IV) hypertension 2. Patients taking ACE inhibitors or Beta Blockers may complain of bad taste in mouth and present with lichenoid reaction of oral mucosa 3. Vasoconstrictor will interact with non-selective Beta blocker, dose reduction guide (relative contraindication) 4. If taking calcium channel blockers (e.g., amlodipine) = gingival hyperplasia 5. Before sending a consult = make sure the patient is actually taking the medication and assess the anxiety and stress of patient to make sure they don’t have “white-coat” HTN (use CDAS) 6. NSAIDs may diminish strength of ACE inhibitors, Beta blockers, and diuretics 7. Opiates decrease effect of diuretics 8. Clarithromycin can’t be used with Ca Channel Blockers, decreases effect of the blocker c. CAD (coronary artery disease) / angina pectoris i. Angina Pectoris = discomfort that occurs when myocardial oxygen demand exceeds the supply, graded by Canadian Cardiovascular Society (CCS) 1. Chronic (Stable) AP = caused by artery obstruction secondary to atherosclerosis, pain that repeats after activities such as climbing stairs a. 50% have normal ECG 2. Unstable AP = recent onset with increasing severity, duration, and frequency. Occurs at rest ii. Clinical Presentation 1. Short duration of pain, shortness of breath, nausea, pressure, tightness iii. Pharm 1. Nitrates 2. Beta Blockers 3. Calcium Channel Blockers (Amlodipine) 4. Aspirin 5. Heparin iv. Non-pharm 1. CABG (coronary artery bypass graft) for left main coronary disease patients, left ventricular ejection fraction

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