Essentials Of Medicine For Dentistry - PDF

ESSENTIALS OF MEDICINE FOR DENTISTRY Dr. Doryck L. Boyd, DDS Oral & Maxillofacial Pathologist Associate Professor  CARDIOVASCULAR DISEASE Dental patient may present with: – Confirmed history of cardiovascular disease (CVD) – Signs and/or symptoms of CVD...

ESSENTIALS OF MEDICINE FOR DENTISTRY Dr. Doryck L. Boyd, DDS Oral & Maxillofacial Pathologist Associate Professor  CARDIOVASCULAR DISEASE Dental patient may present with: – Confirmed history of cardiovascular disease (CVD) – Signs and/or symptoms of CVD – Cardiac emergency may arise in clinic DHCW must be prepared to manage the above  General Critical Management Guidelines Be aware of increased morbidity & mortality Carefully observe for signs/symptoms of undiagnosed CVD Attention to medications (duration, dose)  tell severity & risk of side effects & interactions Close communication with physician a MUST Prevent & control infection a MUST Early morning appointment. Reduce stress  Catecholamine release  BP Safe levels of LA + epinephrine. ASPIRATE  Known Cardiac Patient Congenital Heart Disease: – Ventricular septal defect – Idiopathic hypertrophic subaortic stenosis – Bicuspid aortic valve complex HD (outflow) – Patent ductus arteriosus murmur – Pulmonary stenosis – Tetralogy of Fallot (outflow obstruction  decrease oxygen) – Marfan syndrome – Cortication of aorta  Known Cardiac Patient Management & Considerations: – Increased risk of bacteremia  endocarditis – Antibiotic prophylaxis required Special Considerations: Marfan’s syndrome: 2/3 with congested heart failure, aortic aneurysim rupture  death Turner’s syndrome (women): cortication of aorta Tetrology of Fallot: usually corrected before first dental visit  Acquired Cardiac Disease Mitral valve prolapse Degenerative heart disease Rheumatic valvular disease Asymmetric septal hypertrophy Syphilitic aortic valve disease Endocarditis Management/Considerations: – Medical referral for current status – Antibiotic prophylaxis for Hx of Infective Endocarditis only  Prosthetic Valve Disease Management/Considerations: Very high risk for infective carditis Anticoagulant therapy require special precaution if invasive procedure  bleeding Contact physician: withdraw anticoagulant for 2 days prior to procedure  Angina pectoris Management/Considerations: Implies advanced arteriosclerosis Premedicate with anti-anginal or sedative medications prior to stressful procedures Hypotension after general anesthesia  myocardial infarction Routine dental care for stable cases for last 3 months No elective care with unstable angina  Angina pectoris Management/Considerations (cont): Caution with dose of LA + epinephrine Aspirate while injecting Short morning appointments Minimize stress Monitor BP, heart rate Immediate medical attention should close by.  Recent MI (within 6 mths) Management/Considerations: Implies advanced arteriosclerosis Written consultation with physician advisable Stress  re-infarction May be on anticoagulant or aspirin Require recovery period before elective dentistry (3 – 6 mos) Minimum LA + epinephrine Short, stressless morning appointment Monitor vital signs. Medical help near by.  MI over 6 months & Endocarditis Management/Considerations: Written consultation with physician advisable Stress  re-infarction May be anticoagulant or aspirin therapy Elective dental treatment with limited epinephrine Ensure good pain control  less stress Endocarditis: IV Drug abusers. Exceedingly high risk of recurrent endocarditis.  Arrhythmias (Abnormal heart beat/rate) Management/Considerations: Most need no change in routine dental care May require effective anxiety control Advanced cases  CVA (blindness, irregular speech, decreased limb sensitivity, hemiplegia) Stress or hypoxia (gauze, rubber dam)  increased arrhythmia Limited epinephrine  Arrhythmia Management/Considerations (cont): Monitor Potassium levels if on diuretics to minimize precipitating arrhythmia Cardiac glycoside toxicity with anorexia, loss of appetite, nausea, vomiting & visual disturbance may occur Patients may have pacemaker (caution) Evaluate coagulation state. Coumadin (warfarin), dicumerol, Heparin, cumarin commonly prescribed to prevent strokes. Pacemaker & Congested Heart Failure Pacemaker: Management/Considerations: May imply Hx of bradycardia (slow heart beat) Avoid external electromagnetic devices (electro-surgical units greatest risk) CONGESTED HEART FAILURE: Management/Considerations: Implies advanced heart disease, HBP, CHD, myopathy, valvular disease  high risk of mortality May result in excessive metabolic demand  Congested Heart Disease Management/Considerations Medications and side effects can complicate dental treatment: – Diuretics & Digitalis  nausea + vomiting – Avoid triggering gag reflex Reduce stress. Stress increases workload on heart Treat in reclining chair position. Prone to pulmonary congestion if retained in supine position for too long  Heart Transplant Recipient Management/Considerations: Dental infections should be treated before transplant Medical consultation a MUST Patient may be on immunosuppressive drugs for life  increased susceptibility to infections Cyclosporine  gingival hyperplasia Drug induced xerostomia  increased caries + PDD, & candidiasis  Other Heart Defects Management/Considerations; Arterio-arterial or arterio-venous fistula  endocarditis Streptococccus viridans pericarditis may follow invasive dental treatment Artificial grafts with prosthetic material can be site for hematogenous implantation of bacteria post invasive dental treatment. Prophylactic coverage if graft placed less than 6 months.  HYPERTENSION Management/Considerations Accelerates atherosclerosis  CHF + CVA Cardiovascular complications increase with age if BP is high Renal failure & MI possible Minimal use of epinephrine Side effect of anti-hypertensve drug  postural hypotension, confusion, depression, xerostomia, loss of libido, angioedema, gingival enlargement  HYPERTENSION Management/Considerations (cont) Compliance with meds frequent problem Elective dental Rx deferred if BP not controlled Classification of Blood Pressure ( > 18 y o) Category Systolic Diastolic Normal < 120 and 120  Cardiac Disease SIGNS CONSIDERATIONS Gross obesity Risk for CHD Nicotine/alcohol Risk for CHD Xanthelasma Hypercholesterol  CHD Elevated veins Congested Heart Failure Clubbed fingers Congenital heart Disease – Nail cyanosis CHD Swollen ankles Right side Heart Failure  Cardiac Disease SIGNS CONSIDERATIONS Heart murmur Valvular disease Abnormal BP Hypertension, Congested HD Irregular pulse Atrial fibrillation Chest tightness, pain Myocardial ischemia Dyspnea, SOB Left side HF, Congested HD Orthopnea, SOB recumbent LSHF, CHD Paroxysmal nocturnal dyspnea LSHF, CHD  Cardiac Disease SIGNS CONSIDERATION Severe cramping, claudication Atherosclerosis Xerostomia Side Effects of Orthostatic hypotension antihypertensve Impotence medications Depression Headache Visual blurring Dizziness, light headedness  EMERGENCY CARDIAC PATIENT Familiarity of the classical signs & symptoms of cardiac distress, and appropriate management of emergency are essential. Treatment other than emergencies not within the scope of the DHCW. Angina pectoris: Definition: clinical term referring to brief paroxysmal thoracic pain of moderate intensity resulting from ischemic heart disease  Angina pectoris Etiology: coronary arteriosclerosis or atherosclerotc obstruction of on or more of the 3 major coronary arteries  transient myocardial oxygen demand in excess of the available oxygen supply Clinical Presentation: Effort or stress related substernal pressure Tightness or discomfort which radiates a sense of numbness or tingling to the LEFT shoulder, medial surface arm, jaw, throat or neck  Angina pectoris Emergency Treatment Stop dental Rx, confirm Dx & eliminate precipitating factors. Calmly reassure & make patient comfortable Admin vasodilator (nitroglycerin 0.4 mg tabs sublingual. Repeat q 5 min. X 3 p r n. Admin oxygen (2 – 4 liters/ minute flow) Record vital signs If attack continues, call for help, start IV, summon medical assistance to transport patient to ER  Myocardial Infarction (MI) Definition: Irreversible myocardial damage resulting from prolonged ischemic injury Etiology: Coronary artery atherosclerosis & thrombolytic vascular occlusion  MI Clinical Presentation: Severe prolonged substernal or chest pain Pain radiate to either arm or mandible Nausea, vomiting, sense of impending doom Denial, insistence upon gastric distress  Myocardial Infarction Emergency Treatment Reaffirm diagnosis Summon medical assistance (926-5721) Admin nitroglycerin 0.4 mg sublingually Admin crushed aspirin (325 mg) if not allergic Admin oxygen (2 – 4 liters/minute low) Start IV, admin analgesic (morphine250 mg) & repeat p r n q 10 minutes Monitor & record vital signs Prepare to start CPR  Cardiac Arrest Definition: sudden cessation of cardiac function with disappearance of arterial BP, indicating ventral fibrillation, tachycardia or ventricular stand still Etiology: myopathy or advanced atherosclerosis, coronary artery disease. Clinical Presentation: Mostly respiration arrest precedes cardiac No pulse, BP, heart beat Seizure common  Cardiac Arrest Emergency Treatment: Basic Life Support(BLS) Recognize unconsciousness & confirm Dx Summon medical assistance & initiate ABCs,  CPR, with patient on flat surface Open airway, check for breathing Ventilate with 2 long breaths 1 – 1.5 sec each Check carotid pulse (lateral neck) Initiate external chest compressions 5:1 or 15:2 Arrange for defibrillation ASAP Start IV, transport to ER COMMON MEDS RELATED TO CHD CONGESTED HEART FAILURE  Digitoxin (digitalis) – Limit epinephrine  increase BP – Avoid erythromycin (increase absorption of digitalis) – Avoid barbiturates (increase digitalis metabolism) COMMON MEDS RELATED TO CHD ANTI-ANGINAL Beta-blockers (propranodol) – NSAID may antagonize the anti- hypertensive effect – Decrease clearance of LA Calcium channel blockers (nefedipine) – Epinephrine & NSAIDS antagonize anti- hypertensive effect) – Gingival hyperplasia COMMON MEDS RELATED TO CHD ANTI-ANGINAL (cont) Renin-Angiotensin System (captopril, enalapril) – Concerns same as calcium channel blockers) ANTI-CHOLESTEROL: (Lipitor) atorvastatin (Zocor) simvastin – Erythromycin may cause rhabdomyolysis & acute renal failure.  Infective Endocarditis & Prophylactic Regimens Definition: Severe infection of cardiac valve caused by blood borne pathogens the gain entry thru mouth, GIT, skin, GUT, following surgical manipulation, parenteral (subcutaneous) procedure or automanipulation. Etiology: alpha hemolytic Steptococcus viridans, sanguis, mitior, pneumoniae = 50% of the time. Damage due to immune response (Ab-Ag complexes) Heart Conditions That Predispose Patients to Infective Endocarditis Prosthetic heart valve Pulmonary stenosis Tetralogy of Fallot Ventricular septal defect Congenital heart defects Marfan syndrome Aortic stenosis + regurgitation Mitral stenosis + regurgitation Mitral valve prolapse + regurgitation Previous Hx of endocarditis Patent ductus arteriosis Intravascular shunts  Infective Endocarditis Antibiotic prophylaxis is NOT required: – Uncomplicated atrial septal defect – Coronary bypass surgery > 6 weeks – Pacemakers & cardiac defibrillator – Rheumatic fever & no rheumatic heart disease  Infective Endocarditis Clinical Presentation: Early: (may persists for weeks before diagnosis) – Unexplained low grade fever – Malaise, anemia, lethargy, weight loss – Joint pain Later: (deterioration of cardiac function) – Dyspnea, orthopnea – Heart murmur – Emboli  vasculitis, aneurysim, heart & kidney failure  Infective Endocarditis Common Systemic Manifestations Subungual bleeding Small red splinter-like blood spots under proximal 2/3 nails Osler’s nodes Tender pink red painful lumps in finger & toe pads Roth’s spots Pale retinal hemorrhage Petechial bleeding of skin, mucosa, conjunctiva Splenomegaly & Hematuria (blood in urine)  Infective Endocarditis Diagnosis: – Blood culture  identify microbe – Elevated erythrocyte sedimentation rate (ESR) – Mild anemia, leukocytosis (increased WBC) – Circulating immune complexes Treatment: large doses penicillin (1.2 million units) + streptomycin (500 mg q 12 hrs Fatality rate = 20 – 70 %  Infective Endocarditis Standard Antibiotic Prophylactic Regimen Patient Oral Route Adults, child >66 kg 2.0 g Amoxicillin 1 hr before treatment Adults, child >66 kg 600 mg Clindamycin (allergic to penicillin) 1 hr before treatment. (or 2 gm Cephalexin) Child < 30 kg 50 mg/kg Amoxicillin Child 3 recurrent seizures Convulsion = physical sign of seizure activity  Seizure Disorders Etiology: – Majority of epileptic seizures have no identifiable cause – Developmental anomalies, – Hereditary predisposition – Head trauma – Infections – Metabolic defects – Tumors (vascular malformations)  Non-epileptic Seizures Etiology: – Cerebral ischemia (TIA) – Hypoglycemia (diabetic) – Drugs (cocaine) – Alcohol withdrawal – Barbiturates – Benzodiazepines  Seizure Disorders Clinical finding/presentations: – Epilepsy is common (1% of population) – 30% suffer from genetic epilepsy with primary generalized seizures – 60% of adults suffer from symptomatic partial epilepsies – 40% suffer from childhood epilepsies  Types of Seizures 1. Partial Simple partial (conscious) (focal, Motor symptoms local) Somaticosensory symptoms Autonomic symptoms Psychic symptoms Complex partial (impaired consciousness) Begin as simple partial  impaired consciousness With impaired consciousness at onset Partial seizures evolving to secondary generalized seizures  Types of Seizures 2. Generalized Absence of seizures (convulsive Myoclonic seizures (shock- non-convulsive) like contraction) Clonic seizures (spasm with rigidity & relaxation in rapid succession) Tonc seizures (continuous contraction) Tonic-clonic seizures  Types of Seizures 3. Unclassified: – Cannot be classified because of inadequate or incomplete data – Defy classification (neonatal seizures such as rhythmic eye movement, chewing & swimming movements.  Evaluation of Seizures Ask patients about precipitating factors: Skipping medication Infection Medications Fatigue Stress Skipping meals Anxiety Menses Pain Alcohol  Evaluation of Seizures Ask about: – Aura – Warning signs: Irritability Mood changes Confusion Upset stomach Slurring of speech Frequent blinking or blank stare Blurred vision Auditory, gustatory & olfactory hallucinations  Diagnostic Test for Seizures EEG = electro-encephalo-gram Negative EEG does NOT exclude the diagnosis CT or MRI to find structural causes Lab Tests to R/O other causes of seizures: – Elevated glucose levels – BUN = Blood Urea Nitrogen – Creatinine (end product of creatine metabolism, found in muscle, blood, excreted in urine) – Electrolytes  Most Often Rx for Seizures Medication Usage Side Effects Phenobarbital Tonic/Clonic Drowsiness, CNS depression megaloblastic anemia Phenytoin Tonic/Clonic Confusion, (Dilantin) lethargy, ataxia, gingival HP, skin rash, blood dyscrasias Dental Management of Seizure Patient Controlled seizures  Routine dental care Special Considerations: Concern Management Patients with CNS depression Avoid narcotics Hx lidocaine allergy Avoid usage Foreign bodies in mouth Remove Uncontrolled seizure activity Gently restrain Position on side Lift jaws to minimize aspiration Monitor vital signs  Emergency Care of Seizures Single short seizure  No Rx Postictal stage  Keep under observation Multiple seizures  Continuous seizure for 30 minutes = Status Epilepticus (mortality rate 10-12%) Protracted cases = mortality 77% Rx: slow IV or IM 5 to 10 mg Diazepam (muscle relaxant) until seizures stop  Multiple Sclerosis (MS) Definition: – Degenerative disorder of the CNS – De-myelinated plaques throughout the CNS – MOST common in young adults ( 20–40 y o) Etiology: unknown Clinical finding/presentations: – Progressive weakness of lower limbs – Cerebellar ataxia – Sensory & visual disturbances – Periods of remission  Multiple Sclerosis Management: – May be on steroids (imune supression) – Cushingoid changes – Diazepam to control muscle spasm  Parkinson’s Disease Definition: – Progressive disorder of the basal ganglion – Result of degeneration of nigrostriatal pathway – Common in older adults (1% over 60 y o) Clinical findings/presentations: – Begin with tremors at rest – Rigidity & bradykinesia (sluggish mental/physical response) – Tremors subside with intended movements & sleep  Parkinson’s Disease Clinical findings/presentation (cont): – Common findings: Excessive sweating Drooling with excessive saliva Walking with short shuffling steps Reduced arm swing Speech slurred & monotonous Pill rolling of fingers Blank facial expression Poor blink reflex  Parkinson’s Disease Management: – Fatigue increases tremor – Short morning appointments – Xerostomia due to anti-cholinergic meds that is used to control drooling Medications: – Cogentin (anti-cholinergic) – Anti-spasmodics – 1-dopa  Myasthema Gravis (MG) Definition: – Autoimmune disorder – Transmission defect at neuro-muscular junction – Clinical findings/presentations: Abnormal fatigue of muscles Early sign is ptosis (drooping of eyelids) Muscles of mastication, swallowing & respiration affected  Myasthemia gravis Management: – Weakness increases during the day – Early morning appointments after meds – Main concern is respiratory depression – Xerostomia Treatment: – Neostigmine & pyridostigmine (anti-cholinesterases)  xerostomia PSYCHIATRIC DISORDERS Anxiety = a feeling of all is not well, impending disaster Rx: Counseling Stress reduction Drugs Side Effects Alprazolam (Xanax) Drowsiness Diazepam (Valium) CNS depression Lorazepam (Atrivan)  Depression General emotional dejection & withdrawal 13–18% women , 8–11% men at least 1 episode 3 Types: Normal situational Adjustment disorder reaction Neurotic (chronic) Dysthemia (mental depression) Major depresion Without psychosis With psychosis (mental disorder; deeper, more prolonged)  Depression Clinical findings/presentation: – Lack of personal hygiene – Complains of xerostomia  caries, PDD – Complains of Facial pain syndrome Diagnosis: – History – Physical exam – Signs / symptoms  Depression Treatment Side Effects Tricyclics: Elavil Xerostomia Aventyl Blurred vision Tofranil Sedation, seizures Hypotension, tachcardia Monoamine Potent CNS depression oxidase (MAO) with barbiturate, ETOH, inhibitors analgesics. Cheese, fish, (Marplan) (Nardil) beer may precipitate HP  Depression Treatment Side Effects Selective Headache, tremor, serotonin nausea, diarrhea, uptake insomnia, agitation, inhibitor nervousness, sweating, (SSRI) dizziness, somnolence, (Prozax) anorgasmia (Zoloft) (Paxil)  Manic-Depressive Disorder (Bipolar Affective Disorder) Affective (pertaining to a feeling or mental state) disorder involving manifestations of an individual’s feeling or mood. 1% of population 3 Types: Rx: Lithium (arrhythmia, hypotension) Manic Excessive unceasing & unselective enthusiasm, elation, euphoria Depressive Multiple episodes of depression with at least one manic episode Mixed Mood swings followed by episode of depression  Schizophrenia Definition: Disturbance of thinking, perception with delusions, hallucinations, impaired reality testing. Treatment: Side Effects Neuoleptic Dyskinesia (impaired movement) (Haldol) hypotension, xerostomia, (Moban) avoid barbiturates, narcotics, atropine Phenothiazine (Thorozine)  Panic Disorder Recurrent panic attacks (PAs) without external event Attacks consist of: – Intense apprehension & terror – Sense of imminent danger & urge to escape – Difficulty breathing – Chest palpitations & pain – Dizziness & Sweating  Panic Disorder 60% of patients with PD also suffer from major depression  20% attempting suicide Differential Diagnosis: – Angina pectoris Hyperthyroidism – Pheochromocytoma  increase epinephrine – Excess caffeine, stimulants, sympathomimetics in nasal decongestants – Alcohol or hypnotics withdrawal  Panic Disorder May be associated with Mitral Valve Prolapse (8 – 33%) due to prolong exposure to panic induced increased levels of circulating catecholamines  increased ventricular contraction. Epidemiology; – Begin in late adolescence or early adulthood – Women (worst) > Men – Often lifelong illness – More likely to be recipients of disability payments  Panic Disorder Pathophysiology: – Abnormal cerebral blood flow to amygdala (part of limbic system which regulates mood & emotions)  grossly misinterprets significance of ambiguous bodily sensation. – Amygdala stimulate parabranchial nucleus  fear, fight, flight” response & increased breathing – Amygdala stimulate locus ceruleus  increase epinephrine  increase BP & Heart rate – Amygdala stimulate paraventricular nucleus (Hypothalamus)  autonomic arousal (hypervigilance, exaggerated startle response) + Sterods  Panic Disorder Treatment: Psychotherapy (Cognitive Behavior Therapy) – Educate about disorder & help them recognize & challenge their automatic negative misinterpretation of ordinary physical sensations Selective Serotonin Reuptake Inhibitors (SSRI) – Paxil, Zoloft, Prozac  xerostomia, dysgeusia (altered taste), gingivitis, stomatitis Benzo-diazephines – Xanax, Valium xerostomia, sialorrhea  Panic Disorder Dental Management: Display supportive, non-judgemental attitude & and advise that psychiatric therapy will be confidential. Consultation mandatory. Oral hygiene & artificial saliva  xerostomia Profound anesthesia  reduce stress Avoid: codeine, erythromycin, antihistamine, ketoconazole, muscle relaxant, opioid analgesic.  Dementia Definition: – Impairment of cognitive function and learned behavior. – Progressive mental, motor deterioration – Changes in personality / behavioral patterns.  Dementia 4 Types: Alzheimer 50%. Insidious onset. R/O hypothyroidism TIA dementia Hx of hypertension Pressure Head trauma / meningitis hydrocephalus AIDS dementia Global cognitive loss Treatment: None  Dental Management of Psychiatric Patient Main concern xerostomia due to medication Regular prophylaxis + Fluoride supplements Salivary substitutes + sialagogues (stimulate salivary flow) Patient cooperation & informed consent may be hard to obtain. Due to possible interaction between epinephrine & MAO inhibitors  hypertension MUST aspirate before deposition of LA  Diseases of White Blood Cells Differential WBC Count (Normal Values) Cell Type Number/mm3 Percent Band 0 – 2,000 0- 10 Neutrophil 3000 – 6,000 30 – 75 Lynphocyte 1,500 – 4,000 20 – 50 Monocyte 200 – 900 1 – 12 Eosinophil 100 – 700 0 – 3 Basophil 20 – 150 0–1 Total WBC count = 4,000 – 11,000  Granulocytosis Increase in total circulating WBC Major Causes of Granulocytosis: – Infection – Tissue necrosis – Allergic reaction – Inflammatory disease – Cancer – Leukemia  Major Causes of Increased Neutrophils Bacterial infection Increased Bands (immature neutrophils) Tissue infarction Burns, MI Myelogenous Immature malignant cells leukemia  anemia + infection + thrombocytopenia Stress & Increased epinephrine Exercise Neutrophil count > 7,500 cells/mm3  Major Cause of Increased Lymphocytes Acute viral Infect. mononucleosis, infection viral hepatitis Chronic TB, pertussus, syphilis infection Lymphocytic Abn malignant cells in leukemia blood + lymphadenopathy Lymphocyte count > 4,000 cells/mm3  Major cause of Eosinophilia Allergies Hayfever, angioedema Dermatologic Pemphigus, eczema, serum diease sickness Drug reactions Penicilllin, aspirin, sulfonamides, cephalosporins Fungal Infections Eosinophil count > 700 cells/mm3  Neutropenia Leukopenia: absolute decrease in WBC Causes of Neutropenia (sign of marrow disorder) Drug toxicity Leukemia CT diseases Cancer Rx Metastatic cancer X-ray Rx Hereditary Mild = 1,000 – 2,000 cells/m3 Moderate = 500 – 1,000 cells/mm3 Severe = < 500 cell/mm3 Patients highly susceptible to bacterial infection making dental Rx risky for bacteremia  Lymphopenia Patients highly susceptible to viral & fungal infections (oral candidiasis, 2nd herpes) Major Causes Considerations HIV infection Opportunistic infection, Kaposi sarcoma, weight loss, lymphadenopathy Renal failure Nephotoxic drugs, glomerulonephritis, kidney stones, diabetic nephropathy Immunosuppressive drugsOrgan transplant (prednisone, cyclosporin, azathioprine)  Oral & Dental Significance Severe neutropenia  early oral ulcers (no red halo) Severe neutropenia  increased susceptability to bacterial infection. Severe neutropenia  only emergency dental Rx with multiple broad spectrum IV antibiotics DHCW have important role in preventing serious life threatening infection while patients are neutropenic from chemotherapy. Teeth with advanced PPD treated before chemotherapy.  ANAEMIA Definition: – Decrease hemaglobin (Hb) in blood  decreased oxygen in tissues Oral Signs: – Pallor (Lips & Nails) – Atrophic lingual papillae – Diffuse bone radiolucency on dental radiographs (Sickle cell anemia)  Basic Lab Tests for Anemia TESTS MALE FEMALE Hemoglobin (Hb) 13.5 -17.5 12 –15 Hematocrit (%) (HCT) 40 – 52 36 – 48 RBC count (million) 4.5 – 6.5 4 – 5.5 Mean Corpuscular 80 – 100 80–100 Volume (MCV)(femtoliter) Mean Corpuscular 27 - 34 27 –34 Hemoglobin (MCH) (picogram) (pg) Mean Corpuscular Hb 30-35 30 –35 Concentration (MCHC) (g/deciliter) Reticulocyte (%) < 1.5 < 1.5  Major Causes of Anemia Type Causes Microcytic Hemorrhage, Fe deficiency & malabsorption, heavy menses Macrocytic B-12, Folate,Folic acid deficient Hemolytic Sickle cell anemia, Thalassemia, Glucose-6-phosphate dehydrogenase deficient(G6PD) Autoimmune diseases NormocyticDrug toxicity, Leukemia, metastatic cancer  Aplastic Anemia Definition: – Normochromic, normocytic  leukopenia + thrombocytopenia Etiology: – Chemical agents (benzene, arsenic, acetylbalicylic acid, phenytoin) – Anti-neoplastic drugs (methotrexate) – Ionizing radiation  Aplastic Anemia Oral Manifestations – Pallor – Petechiae, purpura – Gingival bleeding without cause – Ulcers without red halo due to neutropenia Dental Considerations: – Beware of procedures that cause bleeding – Infection control – Keep procedure to a minimum  Pernicious Anemia Etiology: B12 deficiency due lack of intrinsic factor (secreted in stomach) Oral Manifestations: Tongue – Painful Loss of taste – “Fire-red” at tip & margins – Loss of filliform papilla (“bald”) Increased infections Difficulty tolerating dentures Mucosa + skin  greenish-yellow color  Pernicious Anemia Differential Diagnosis: – Mechanical irritation – Syphilitic glossitis – Glossopyrosis (Burning tongue syndrome) – Psychotic pain – Allergic reaction Dental Considerations: Same as aplastic anemia  Glucose-6-phosphate Dehydrogenase Deficiency Definition: – X linked black males (homozygous female) – G6PD = key enzyme in reduction reactions occurring RBC  essential for cellular integrity Etiology: – Aspirin – Phenacetin (Tylenol)  Acute hemolysis – Dental infection  Sickle Cell Anemia Definition: – Chronic hemolytic anemia mostly Blacks – Valine substituted for glutamic acid in the 6th peptide of beta chain = HbS – HbS less soluble  semisolid gel  rod-like tactoids  sickling of RBCs unable to pass thru capillaries  Sickle Cell Anemia Oral Manifestations: – Pallor – Jaundice (yellow) – Delayed eruption – Hypoplastic secondary dentin – Increased radiolucency (decreased bone trabeculae) especially in alveolar bone between roots, due to increased erythropoiesis  “step ladder” effect  Sickle Cell Anemia Oral Manifestations (cont): – Thick lamina dura – Vascular occulsion  osteomylitis paresthesia of mental nerve – Skull: Thick diploe (loose osseous tissue between 2 layers of cranial bone) Trabeculae run perpendicular to layers  “hair on end” pattern Similar skull features seen with Thalassemia  Sickle Cell Anemia Dental Considerations: – Avoid prolonged & extensive surgery of soft tissues – Good oral hygiene – Infection  aplastic anemia + death – Avoid general anesthesia (also patients with trait)  Hemophilia Definition: Bleeding disorder, sex linked  only males Inherited deficiency of coagulating factors Mostly V111 Hemophilia A von Willebrand’s ds 1X = Hemophilia B Signs/Symptoms: Serious hemorrhage from trivial injuries Hematomas + Hematuria (blood inurine) Epistaxis + GI bleeding  Hemophilia Dental Considerations: Periodontics: Conservative, no surgery Restorative: – Use rubber dam to protect soft tissues. Epinephrine impregnated retraction cord Anesthesia: NO LA without factor V111 replacement. Blocks are risky due to possible bleeding into facial planesairway obstruction Nitrous oxide OK. No intubation  Hemophilia Dental Considerations (cont) Oral surgery: Use local hemostatic agents (oxidized cellulose + bovine thrombin NaCO3) Use mechanical splints, Use smallest sutures Replace factor V111 Endodontic: Pulpotomy on primary teeth OK. 1:1,000 epinephrine to control bleeding Prosthodontics: OK MUST have good oral hygiene  Polycythemia vera Definition: – Chronic life shortening myeloproliferative (blood forming) disorder – Increased RBCs  increased Hb levels Signs/Symptoms: – Fatigability – Difficulty concentrating – Headaches – Drowsiness  Polycythemia vera Oral Manifestations: – Mucosa (also ears)  purplish-red, petechia – Tongue  crystal violet – Gingiva  swollen, bleeds easily – Extraction (surgery)  severe bleeding Dental Considerations: – Must do Hb, WBC, platelet count (especially if recent radioactive P prescription) – If RBC count high  severe bleeding – Good oral hygiene  Platelet Disorders Normal platelet count = 150,000 – 400.000 mm3 Thrombocytosis = increased platelets – Etiology: Polcythemia Infection Neoplasms Exercise Pregnancy Epinephrine release  Platelet Disorders Thromboctopenia: < 140,000 mm3 – < 75,000 mm3 post surgical hemorrhage – < 25,000 mm3 spontaneous hemorrhage easy bruising, petechiae + ecchymosis into skin & mucosa  Major Causes of Thrombocytopenia Drug reactions Cancer chemotherapy Leukemia Idiopathic thrombocytopenia purpura Viral infections Autoimmune diseases  Thrombocytopenia Oral Significance: (May be early signs) – Petechiae – Ecchymosis – Spontaneous gingival bleeding Dental Significance: – Medical consultation needed – Platelet transfusion prior to invasive procedures if count < 50,000 mm3  Screening for Bleeding Disorders Important Questions in Medical History: Frequency of abnormal bleeding History of severe epistaxis Increased menstrual bleeding Recent spontaneous bruising Severe gingival bleeding Post surgical hemorrhage Post extraction hemorrhage Date of recent chemotherapy  Screening for Bleeding Disorders Drug History: Aspirin (NSAIDs)  depress platelet function Cell Life Span RBC 60 – 120 days WBC 7 – 10 hours Platelet 9 –12 days  Screening for Bleeding Disorders Physical signs: – Petechiae – Ecchymosis – Telangiectasia – Spider angioma Associated Diseases: – Anemias Leukemias – Renal disease Hepatic disease  Tests for Bleeding Disorders Prothrombin Time Measures extrinsic (PT) coagulation pathway Prolonged with deficiencies in factors 11, V, V11 X, fibrinogen Activated partial Measures intrinsic Thromboplastin Time pathway (APTT) Detects deficiencies in factor 11, V, V11, 1X, X, X1, XV1  Tests for Bleeding Disorders Thrombin Time Detects circulating (TT) inhibitors, decreased fibrinogen & dysfibrinogenemia Bleeding Time An in vivo test for clot (BT) formation Detect platelet defect, von Willebrand disease, thrombocytopenia  Bleeding Disorders Not Detected with Screening Tests Mild hemophilia Deficiency of factor X111 Hereditary hemorrhagic telangiectasia (HHT) Senile purpura Cushing’s syndrome Mild von Willebrand disease  Management of Bleeding Disorders Medical consultation – Primary care physician – Internist – Hematologist  PULMONARY DISEASE CHRONIC AIRWAY DISEASE: – Bronchial asthma – Chronic Obstructive Pulmonary Disease – Emphysema – Chronic obstructive bronchitis – Other: – Simple chronic bronchitis – Bronchiectasis  Bronchial Asthma Definition: – Increased tracheo-bronchial hypersensitivity – Bronchial edema & narrowing of airway – Hyper-secretion of mucus – Diminished ciliary activity – Increased bronchial infections – Epidemiology:  Bronchial Asthma Medical management: – Goal = prevent occurrence of attacks – Minimize frequency & severity of attacks – Identify & avoid of precipitating factors – Patient education & compliance with Rx Medications: – Sympathomimetic bronchodilator (inhaled) – Xanthine preparations – Steorids  Bronchial Asthma Extrinsic (Allergic) Intrinsic Allergic stimuli Idiopathic Allergic history No allergic history Elevated IgE Normal IgE Positive skin test Normal skin test Childhood onset Adult onset Seasonal variation No seasonal change Intermittent attacks Continuous attacks Note: 50 - 80 % of cases have features of both  Bronchial Asthma Clinical Triad: – Wheezing – Coughing – Dyspnea (difficulty breathing) Acute asthma attack: – Begin with non-productive cough + wheezing – Tightness in chest (normal rate of breathing) – Resolves in minutes with or without Rx  Bronchial Asthma Severe asthma attack: Begin as an acute attack Increased dyspnea Increased orthopnea (difficulty breathing except in upright position) Use of accessory muscles for respiration Paradoxical pulse (weakness or disappearance of arterial pulse during slow respiration) “Silent chest” (wheezing stops)  respiratory failure  Bronchial Asthma Status asthmaticus: Attack persists for hours/days despite therapy Patient in status asthmaticus show signs of: – Fatigue – Dehydration – Peripheral vascular shock – Drug intoxication Medical Management of Severe Asthmatic Attack Goal of Rx = reverse bronchospasm Administer oxygen at 2 – 3 L/min Prevent dehydration (oral fluids or IV) Administer inhalation sympathomimetic  broncho-dilation Administer steroids  decrease inflammation  decrease obstruction Administer antibiotics if sputum is purulent  Bronchial Asthma Patient Risk Status Low = infrequent attacks + no chronic Rx Moderate = intermittent attacks + chronic Rx Significant = frequent attack in spite of chronic Rx High = symptomatic at time of dental appointment  Specific Guidelines Based on Patient Risk Status Low: No modification of normal Treatment Plan Moderate Steroid supplementation may be advisable if possible adrenal suppression Antibiotic prophylaxis if taking systemic steroid and significant tissue manipulation is needed  Basic Guidelines Based on Patient Risk Status Significant Medical consultation before treatment Sedation should be used when appropriate Steroid supplementation Antibiotic prophylaxis Hospitalization for multiple extractions or advanced surgical procedure High  Emergency treatment only with medical consultation  To Prevent an Asthmatic Attack in Clinic Minimize stress Develop good rapport & openness with patient Sedation if indicated Short morning appointments Patient MUST bring Rx to clinic  Emergency Management of an Asthmatic Attack in Clinic If an emergency arises: Stop dental treatment Comfortably position patient Administer aerosol inhaler (measured dose inhaler are FIRST LINE for Albuterol or Ventolin) Administer oxygen 2 – 3 L/min Call physician if indicated  Emergency Management of an Asthmatic Attack in the Clinic If attack is refractory to patient’s medication: Administer epinephrine 1: 1000 0.3 – 0.5 ml. Repeat dose at 20 minute intervals p.r.n. (Caution if patient over 40 years of age) Establish IV Administer 100 mg Solu-Cortef IV Transfer to medical facility  Special Considerations for Asthmatic Patients Epinephrine Minimize usage (may potentiate cardiac side effect of bronchio- dilator) Aspirin (NSAIDs) Avoid usage (may precipitate broncho-spasm) IV barbiturates Avoid usage (may precipitate attack or laryngo-spasm)  Special Considerations for Asthmatic Patients Erythromycin Avoid usage & Clindomycin (slows theophylline metabolism & causes toxicity with methyxanthine) Candidiass Examine for lesions (due to steroid Rx) Antifungal Rx Contact dermatitis Examine for erythema & sweeling  Chronic Obstructive Pulmonary Disease (COPD) Definition: Obstructed air flow during respiration Chronic bronchitis & Emphysema mostly Etiology: Cigarette smoking (80 – 90% mortality in men & women) Chronic exposure to environmental & occupational pollutants Alpha-1-antitrypsin deficiency (recessive gene)  Chronic Bronchitis Irreversible narrowing of bronchial airway Due to: – Chronic infection – Increased mucous production – Edema of bronchial mucosa – Reduced ciliary activity  Chronic Bronchitis Clinical signs/symptoms: – Hypoxia (reduces oxygen to tissues) – Carbon dioxide retention – Cyanosis (bluish color of skin + mucosa) – Respiratory acidosis – Polycytemia – Pulmonary hypertension – Cor pulmonale (hypertrophy right ventricle) – Heart failure  Emphysema Emphysema = “air in tissues” Irreversible enlargement of bronchioles & alveoli distal to terminal bronchiole Destruction of alveolar walls Collapse of terminal bronchiole Expiration hindered Lung become over inflated (air trapped in lung)  Clinical Features of COPD Chronic bronchitis Emphysema Chronic productive No cough cough Copious, purulent No sputum sputum Noisy chest Quiet chest (rales, rhonchi) Normal chest size “Barrel chest” Chest x-ray normal X-ray show over inflated lung & small heart  Clinical Features of COPD Chronic bronchitis Emphysema Mild to moderate Severe dyspnea dyspnea Frequent respiratory Few infections I infections Hypoxia No hypoxia Cyanosis No cyanosis Polycythemia No polycythemia “Blue blooter” “Pink puffer”  Treatment of COPD No cure Try to reduce effects of lung/vascular damage Goals of Treatment: – Relief of reversible part of airway obstruction – Control cough & level of secretions – Eliminate & prevent respiratory infections – Increase exercise limits of patient – Avoid aggravating factors – Counteract anxiety or depression often seen in these patients Medical Management of COPD Maintenance Therapy Educate patient re disease & its maintenance Bronchodilators Steroids Oxygen Antibiotics Physical therapy Immunization against influenza & pneumonia Digitalis & diuretics Medical Management of COPD Acute Therapy Oxygen (maintain blood PO2 @ 60 mm Hg) Broncho-dilators (open airways, prevent spasm) Antibiotic + steroids Physical therapy (dislodge mucus, promote postural drainage, especially in cases of bronchiectasis)  Clinic Evaluation of COPD Patient Forced Vital Capacity: Have patient take a deep breath Exhale through mouth as rapidly as possible Patient with normal pulmonary function will finish exhaling in less than 5 seconds COPD patient will still exhaling after 5 seconds  Clinic Evaluation of COPD Patient Breath Holding Test Test patient’s functional reserve Take a deep breath & hold nostril closed Length of time before patient must exhale and take another breath indicates degree of pulmonary compromise – 20 seconds or more  low risk patient – 10 – 20 seconds  moderate risk patient – 10 seconds or less  high risk patient  Special Considerations for COPD Patient Concern Management Inability to tolerate Early morning appointment stress Sedation technique in moderate risk patient Respiratory difficulty Humidified Oxygen for exacerbated by Rx low to moderate risk cases Depression of Avoid Nitrous oxide respiration High oxygen Rx Sedatives Tranquilizers Narcotics  Special onsiderations for COPD Patients Concern Management Reduction of vital Avoid fully reclined chair capacity due to reclined position Aggravation of Avoid anti-cholinergic bronchial drugs that dry bronchial inflammation secretions and possible Avoid elective dentistry pneumonia during period of acute exacerbation or respiratory infection  Special Considerations for COPD Patients Concerns Management Methylxanthine Avoid erythromycin & toxicity clindamycin Cardiac stress Minimize or avoid epinephrine if heart disease is also present or patient using bronchiodilators with beta-1 effects Avoid elective treatment during hot & humid weather  Medications for COPD Drug Nebulizer Metered Dose Albuterol Acute Bronchio-spasm or Ventolin 2.5 mg – 5 mg 4 – 8 puffs (salbutamol) USUAL Q 15 – 20 min X 3 (Increase to 1 puff q 30 – 60 sec if needed) Stable asthma/COPD 2.5 mg (1 nebule) 2 puffs USUAL q 6 Hrs p r n Ipratropium COPD 1 – 2 ml(250 –500mg) 2-4 puffs Q6–8 Hrs  Cystic Fibrosis Autosomal recessive Abnormal viscid secretions  plugs Main sites: – Lung  chronic infections, bronchiectasis, respiratory failure – Pancreas  diabetes – Liver  biliary obstruction & cirrhosis – GIT  obstruction – Gall bladder  stones  Cystic Fibrosis Signs/Symptoms: Chronic productive cough Purulent sputum Persisting dyspnea Wheezing Weigh loss, malnourished  retarded growth Bulky offensive stool & diarrhea Abdominal pain Chronic sinus infection  Cystic Fibrosis Oral Manifestations: Submandibular gland  enlarge, reduced saliva Parotid gland  normal Saliva – Elevated protein & enzymes – Increased calcium & phosphate – Normal sodium & potassium Eosinophilic plugs in salivary gland ducts Increased calculus formation Oral Pseudomonas aeruginosa  lung infection  Cystic Fibrosis Diagnosis: – Abnormal sweat test with increased NaCl Medical Treatment: – Control pulmonary infection – Antibiotics & physiotherapy – Monitor nutrition & dietary supplement Oral Management: – Good oral hygiene to reduce calculus & incidence of pneumonia  Type 1 Hypersensitivity Reaction Urticaria: local wheals & erythema on skin Angioedema: larger & deeper edematous area on the skin or mucosa Anaphylactic shock: (previously sensitized) – Acute, explosive systemic reaction – Urticaria Vomiting – Respiratory distress Diarrhea – Vascular collapse – Abdominal cramps  Type 1 Hypersensitivity Reaction IgE mediated Cytokines released from basophils & mast cells – Histamine  itching – SRS-A (slow reactive substance) – ECF (eosinophilic chemotactic factor) Reactions: – Vasodilation  increased permeability – Smooth muscle contraction  asphyxiation  Type 1 Hypersensitivity Reaction Role of Eosinophilia: – Allergic (extrinsic) asthma – Seasonal rhinitis – Systemic anaphylactic shock Examples: – Insect stings Food/drug allergies Diagnostic Tests: – Direct skin test – RAST (radioallergsorbent test)  Type 2 Hypersensitivity Reaction Cytotoxic reaction Complement (C3) dependent Antibody react with antigenic component of cell Examples of injury by Ab to Ag component of CELL – Systemic lupus erythematosis – Coombs-positive hemolytic anemia – Ab-induced thrombocytopenia  Type 2 Hypersensitivity Reaction Example of Ag as part of TISSUE – Graft rejection – Goodpasture’s syndrome: Ab against glomerular & alveolar basement membrane Diagnostic Test: – Detect Ab or complement on cell or tissue – Detect Ab to Ag (cell/tissue) in serum  Type 3 Hypersensitivity Reactions Immune complex reactions Deposition of soluble Ab-Ag complexes in vessels or tissue Examples: – Systemic lupus – Rheumatoid arthritis – Serum sickness due to serum, drugs, HbSAg – Glomerulonephritis Diagnostic Test: Direct immunofluorescence (IF) for Ag, IgG or C3  Type 4 Hypersensitivity Reaction Cell mediated delayed reaction Cells become sensitized after contact with Ag Examples: – Contact dermatitis (poison ivy) – Allograft ( same species) rejection – Granulomas due to intracellular organism (TB) Diagnostic Test: Patch test = Ag applied to skin, left for 48 hrs. Positive if erythema, induration (hardness) or vesicle develop.  ADRENAL GLAND DISORDERS Adrenal glands are located on top of the kidney Consists of outer cortex & central medulla Medulla  catecholamine + epinephrine Cortex (3 parts) Zona glomerulosa (outermost)  aldosterone (mineralocorticoid) Zona fasiculata (central)  cortisol (glucocorticoid) Zona reticularis (innermost) estradiol + testosterone (sex hormones)  Addison’s Disease Hypoadrenocorticism Progressive destruction of the cortex Chronic deficiency in steroid hormones need for gluconeogenesis (fat/protein  carbohydrates) & mineral metabolism Cholesterol  all steroid hormone Anterior pituitary  Adrenocorticotropic hormone (ACTH)  release of steroid hormones  Factors Contributing to Addison’s Disease Tuberculosis (President John Kennedy) Autoimmune destruction of adrenal cortex Neoplastic destruction of adrenal cortex Adrenal infaction Hemorrhage (trauma) of adrenal gland Adrenalectomy Anterior Pituitary disease Sarcoidosis, fungal infections, drugs  Signs & Symptoms of Addison’s Disease Oral melanotic macules Dark pigmentation & fragility of skin Muscle wasting & weakness Fatigue & fainting spells Nausea & vomiting & diarrhea Mental irritability & psychological disturbance Anorexia Hypotension  Laboratory Findings in Addison’s Disease Serum Potassium Increase Blood urea nitrogen Increase HCT Increase Eosinophilia Increase Lymphocytes Increase Plasma/urine cortisol Decrease Serum Sodium Decrease Fasting blood glucose Decrease  Medical Management of Addison’s Disease Replace: GlucocorticoidsSex hormones – Mineralocorticoids Rx: Hydrocortisone 20 – 30 mg – 2/3 dose in morning 1/3 dose late afternoon Dental Management: Medical consultation is mandatory NOTE: dosage of glucocorticoids should be increased in cases trauma, stress, surgery, pain, & infection  Cushing’s Syndrome Hyper-adrenocorticism (excess steroid hormone) Contributing Factors: – Chronic exogenous glucocorticoid Rx – Excess production of ACTH – Elevated endogenous cortisol production – ACTH producing adenoma of pituitary gland – Ectopic production of ACTH from malignant tumor (lung, thyroid, kidney, pancreas)  Clinical Findings in Cushing’s Syndrome Moon facies Buffalo hump (back) Central abdominal obesity Large abdomen Thin extremities Easy bruising Headache Hypertension Hirsutism Hairyness) Osteoporosis Acne Loss of Amenorrhea cortical bone  Laboratory Findings in Cushing’s Syndrome Plasma cortisol Increased Urine cortisol Increased Plasma ACTH Increased Fasting blood glucose Increased Hematocrit Increased (mild) ACTH infusion Increased Serum sodium Decreased Serum potassium Decreased Eosinophilia Decreased Lymphocytes Decreased  Cushing’s Syndrome Medical Management: – Surgical removal of adrenal/pituitary tumor – If bilateral adrenalectomy  life long oral steroid Dental Management: – Medical consultation mandatory – Need to know: Type of steroid Rx Dose Need for supplementation  Corticosteroids Patients on daily steroid Rx often seen by DHCW Need to know how they respond to: – Stress related to dental procedures – Anxiety related to dental procedures – Post-op pain from dental procedures Inappropriate management  potentially life threatening acute adrenal insufficiency aka (Addison’s crisis): Profound asthenia(weakness) Severe pain(abdomen, back, legs) Peripheral vascular collapse  azotemia  Common Uses for Systemic Corticosteroids Endocrine disorders (adrenal insufficiency) Rheumatoid arthritis Systemic lupus erythematosus, Sarcoidosis Pemphigus, pemphigoid, Lichen planus, Erythema multiforme COPD (asthma) Thrombocytopenia, acquired hemolytic anemia Ulcerative colitis, regional enterits (Crohn’s disease)  Special Considerations re Corticosteroids Exacerbation of systemic conditions: – Hypertension GI ulcers – Diabetes mellitus Secondary infections – Osteroporosis Reactivate TB – Cataracts Common initial complaints: – Frequent urination Sleeplessness – Excess appetite Agitation  Corticosteroid Therapy Most adverse reactions occur after a 2 week period General rule = higher dose for short period Topical steroid with low potency agents for oral lesions are safe for short term therapy Ultra-potency topical steroids  potential systemic absorption with open lesions  Systemic Equivalent Doses for Glucocorticoids Hydrocortisone 20 mg Cortisone 25 mg Prednisone 5.0 mg Methylpredisone 4.0 mg Triamcinolone 4.0 mg Dexamethasone 0.75 mg  Relative Topical Steroid Potencies Ultra potent Clobestasol ppropionate 0.05 % Halbetasol propionate 0.05 % Potent Fluocinonide 0.05 % Dexamethasone 0.25 % Moderate Triamcinolone acetonide 0.5/0.1 potent Betamethasone dipropionate 0.05 Mildly Hydrocortisone 1.0% or 0.5 % potent  Steroid Supplementation Guidelines Most patients on chronic steroid Rx can undergo routine dental therapy without supplementation if pain & anxiety are well controlled Patients on chronic steroid Rx may be at risk for adrenal suppression (immuno-suppression) Medical consultation a MUST to assist DHCW to determine need for steroid supplementation  Steroid Supplementation Guidelines Routine dental Suppl not necessary if procedures currently taking steroids. including Good LA & post-op pain extractions control. with LA Admin normal dose on day of procedure if regular steroid usage discontinued within the previous 2 weeks. No suppl if regular steroid usage was stopped for > than 2 weeks or using topical or inhalation steroids.  Steroid Supplementation Guidelines Extremely If currently on steroids & much anxious post-op pain expected, double patient dose on day of procedure and with LA day after. & Complicated Double dose on day of procedure or stressful if regular steroid usage stopped procedure within previous 2 weeks. with LA No suppl if regular steroid usage discontinued for > 2 weeks  Steroid Supplementation Guidelines Dental Admin parenteral (injection) procedures 100mg hydrocortisone 1 hour with before procedure & double general daily dose the following day, anesthesia if post-op pain is expected. Alternate Treat patient on day they usually day take steroid medication. regimen No change in steroid regimen  Thyroid Gland Disorders Bi-lobed thyroid gland Located in midline of neck Inferior to cricoid cartilage Superior to supra-sternal notch Hormones produced: – Tri-iodo-thyronine (T3) – Thyroxine (T4) – Calcitonin (calcium metabolism)  Thyroid Gland Disorders Gland + iodine  thyroglobulin  T3 + T4 Ant pituitary  TSH  T3(8ug) + T4(80) daily Auto-immunity MOSTLY  thyroid disorders Hypo-thyroidism (deficiency of hormones) – Cretinism (infants): skin thick, cool, dry, wrinkled. Macroglossia, thick lips, open drooling mouth. Broad face, short upturned nose. Feet & hands puffy. Mental retardation. – Myxedema (adolescent & adult)  Hypothyroidism Definition/Etiology Hashimoto’s thyroidism – Auto-immune lymphocytic infiltration – Mostly females (10:1) Ave age 30 to 50 – Increased risk for lymphoma Iatrogenic 131 Iodine Rx or surgery Congenital  cretinism Drug induced (Lithium) Hypothalamic or pituitary dysfunction Hypothyroidism: Lab Findings & Diagnostic Tests Chemical Tests: Total T4 (4 – 11 ug/dL) Decreased Free T4 (0.9 – 2.4 ng/dL) Decreased Serum T3 (23 – 25 %) Decreased FTI (0.8 – 2.4 mg/dL Decreased (free thyroxine index) TSH (< 10 ug/ml Increased (Decrease) RAIU (5 – 30% admin dose) Decreased (radioactive iodine uptake) Hypothyroidism: Lab Findings & Diagnostic Tests Antibodies: – Anti-microsomal Ab = + Hashimoto’s disease – Anti-thyroglobin Ab = confirms Hashimoto’s Epidemiology: – 1.4 % adult female 0.1% adult male – Cretinism = approx 1 in 4000 births  Hypothyroidism Clinical Findings/Presentations: Decreased sweating Edematous face Thick edematous skin Macroglossia Diffuse coarse hair Hoarse slow speech Weight gain Bradycardia Elevated TSH Macrocytic anemia T4 uptake low Radio- iodine uptake low Dementia  Hypothyroidism Medical Management: Rx Synthroid Dental Management: Untreated patients very sensitive to following drugs due to CNS depressive effects: – Narcotics Barbiturates Tranquilizers Hypothyroid coma: Symptoms: hypothermia, URT acidosis Emergency Rx: (headache, increased ph & CO2) – Endogenous warming of patient Parenteral T3 & T4 CPR if necessary  Hyperthyroidism Increased hormones  Graves’ disease & diffuse non-toxic goiter Women 4 – 7: 1 Ave age 40 Lab findings/Diagnostic tests: Total T4 Increased Free T4 Increased Serum T3 Increased FTI Increased TSH increased (Decreased) RAIU Increased  Hyperthyroidism Antibodies: – anti-TSH receptor Ab + in Graves’ disease Epidemiology: 1.9 % female 0.2% male Clinical Findings/Presentation: Exophthalmia (bulging eyes) Irritability Psychosis Weight loss Nausia Intolerance to heat Vomiting Insomnia Polyphagia Anxiety (gluttony)  Hyperthyroidism Medical Management; – Surgery (sub-total thyroidectomy – Anti-thyroid drugs (propyl-thiouracil or 131I) Dental Management: Highly sensitive to epinephrine Infection, stress, trauma, pain, surgery  Hyperthyroid Crisis (thyroid storm) Symptoms; High fever, tachycardia Emergency Rx: Cold packs, IV fluids (glucose) Admin hydrocortisone 100 – 200 mg IM/IV  Diabetes mellitus Definition: Sustained high blood glucose level resulting from absolute or relative lack of insulin or decreased responsiveness of peripheral insulin receptors. Classification of Diabetes Type 1 Insulin dependent (IDDM) Type 11 Noninsulin dependent (NIDDM Gestational diabetes (due to pregnancy) Other types due to Pancreas & Hormonal disease or drugs  Diabetes 90% of diabetics seen by DHCW = Type 11 Type 11 managed by diet, exercise, oral hypo- glycemic medication & Rx PDD Complications: Ketoacidosis (most serious) Retinopathy (blindness 25 times more likely) Neuropathy Nephropathy (dialysis 17 times more likely) Microangiopathy gangrene (amputations 5X) CHD twice as likely  Diabetes Etiology: Genetic pre-disposition Destruction of islets of Langerhans (pancreas) Long term steroid medication Hyperthyroidism Hyperpituitarism Epidemiology:  Signs & Symptoms of Diabetes (Worst in Type 1) Polydipsia Marked irritability Polyuria (nocturia) Headache Polyphagia Drowsiness Weight loss Malaise Loss of strength Impotence Blurred or decreased vision Repeated skin/nail infections Paresthesia Postural hypotension Vulvular pruritis  Diabetes Evaluation: Inquire about the following: Age of onset Usual level of blood glucose Frequency of blood & urine test for glucose Type & dose of hypo-glycemic medication History of emergency room visits for ketoacidosis or hypoglycemia (good profile of patient’s disease and compliance of patient in management of their disease)  Diabetes Oral Findings in Poorly Controlled Patients Increased caries Increased gingivitis & periodontal disease Increased candidiasis Xerostomia Increased glucose in saliva Increased susceptibility to infection Delayed healing  Diabetes Clinical Finding IDDM NIDDM Percentage 5% 95% Age of onset 15 40 + Body build Thin Obese Severity Severe Mild Insulin required 100% 25 – 30% Oral hypoglycemic Ineffective 50% respond Ketoacidosis Common Uncommon Rate of clinical onset Rapid Slow Control of disease Unstable Stable  Diabetes Insulin type Effect begin Max Action Time Short acting (hrs) (hrs) (hrs) Regular 1/4 4-6 6-8 Semilente ½ 4-6 12-16 Intermediate acting NPH 3 8-12 18-24 Lente 3 8-12 18-24 Long acting PZI 3-4 14-20 24-36 Ultralente 3-4 16-18 30-36  Emergencies Associated With Diabetes Predisposing Hyperglycemia Hypoglycemia Factors (diabetic acidosis) (insulin shock) Onset Gradual (days) Sudden(mins) Insulin level Insufficient Excessive Dietary intake Norm-Excessive Inadequate Skin Dry/Flushed Moist/Pale Mouth Dry Excess saliva Thirst Intense thirst Absent Breath odor Acetone (sweet) Normal Tremors Absent Frequent  Emergencies Associated With Diabetes (cont) Clinical Hyperglycemia Hypoglycemia Hunger Loss of appetite Hunger Vomiting Common Rare Abdominal pain Frequent Absent Respiration Exaggerated Shallow Blood pressure Low Normal Heart rate Weak/Rapid Full & Bounding  Management of Emergencies Associated With Diabetes Hyperglycemia (diabetic acidosis) – Admin insulin – Patient responds gradually – DHCW provide basic life support (BLS) – Obtain medical assistant Hypoglycemia (insulin shock) – Give oral glucose (if patient is conscious) – IV dextrose (50%) solution or IM glucagon – BLS & request medical assistance  Dental Management of Diabetic Patient Minimize Stress: – Short mid-morning appointments – Sedation (Nitrous oxide or diazepam) Dietary Instructions: – Have normal dietary intake prior to visit – Avoid extending appointment into patient’s normal meal or snack time – Interrupt procedure for glass of orange juice  Dental Management of Diabetic Patient (cont) Minimize Risk of Infection: – Frequent recall oral exams & prophylaxes – Treat periodontal disease aggressively – Postoperative antibiotic prophylaxis for surgical procedures – Infection may increase need for insulin. Consult with physician – Antibiotics for treatment of suppurative periodontitis  Pituitary Gland Disorders Associated with adenomas, craniopharnygioma, metastatic disease. Hypo-pituitarism (Simmond’s disease) Clinical: Symmetric dwarfism Oral Manifestations – Retrognathic mandible (severe Class 11) – Fine wrinkles around mouth & eyes – Delayed eruption – Short roots  Pituitary Disorders Hyper-pituitarism Gigantism (if growth is occurring) Acromegaly (after puberty) Clinical: – Hand/Feet broaden “spade-like” (increased CT) – Skin thicken  increased folds, sweating – Hypertrophy of nasal & aural cartilage – Cranium thickens  prominent ridges Oral Manifestation: – Prognathism (marked Class 111) – Spacing of teeth Macroglossia Hoarseness  Amyloidosis Amyloid – Protein – Light microscopy show amorphous homogeneous eosinophilc material – Congo red stain  apple-green birefringence with polarized light Primary systemic amyloidosis (myeloma) Secondary (reactive) amyloidosis (chronic infections) Rx: dimethyl sulphoxide (foul smelling)  Oral Manifestations of Amyloidosis Macroglossia (50%) tongue firm & indurated Yellow nodules on face, tongue (lateral border) Oral petechiae & ecchymosis Hemorrhagic bullae on tongue  ulcers Xerostomia due to salivary gland involement Claudication (lameness) of muscles of mastication  Lipidosis Gaucher Disease: Deficiency of enzyme beta-glucosidase Acute infantile form  death in first year Adult form  neurological complications Clinical presentation Yellow pigmentation of skin, mucosa & conjunctiva Oral manifestations: – Circumscribed radiolucencies in jaws – Tooth extractions in these areas  bleeding  Lipidosis Niemann-Pick Disease (sphingomyelin lipidosis) Deficiency of enzyme sphingomyelinase Clinical presentation Neurologic complications (severe) Hepato-splenomegaly Physical & mental retardation Symptoms in first few months  death by age 3 Oral manifestations: “Foam-cells in dental pulp  Mucopolysaccharidosis Sanfillippo syndrome Deficiency in enzyme heparin sulphate (type 1) Deficiency in enzyme Nacetyl-alpha-D- glucosaminidase (type 11) Clinical presentation: Severe mental retardation Oral manifestations: Obliteration of dental pulp chamber by irregular dentin  Mucopolysaccharidosis Morquio syndrome Deficiency in enzyme galactosamine-6-sulphatase Clinical: Dwarfism Thick lip Spinal deformity Short neck Broad nose Deafness Corneal clouding Oral Manifestations: – Marked enamel hypoplasia (buccal pittting) – Teeth gray & small NUTRITIONAL DISORDERS PROTEIN DEFICIENCY Marasmus (general starvation) Re-utilization of amino acids from child’s own tissues  synthesis of albumin Clinical: Infants remain alert Kwashiorkor (protein malnutrition) Clinical: Decreased albumin  edema (big belly) Child lethargic & apathetic &” flaky” skin Oral: bald macroglossia angular cheilitis perioral pigmentation xerostomia CHD  Nutritional Deficiency VITAMIN A DEFICIENCY: Animal fat, milk, green leafy vegetables Oral manifestations – Increased oral mucosa keratinization – Metaplasia of salivary ductal epithelium – Xerostomia  altered taste & smell – ? Increased risk of oral carcinoma Vitamin A excess: – Atrophy of oral mucosa Gingivitis – Scaling of lips ?”white squall”)  Nutritional Deficiencies VITAMIN D DEFICIENCY: Rickets (child) Osteomalacia (adult) Defective mineralization of organic matrix  “bow legs” Not critical for amelogenesis or dentinogenesis Vitamin D resistant rickets: (renal tubule Oral manifestations: disorder) – Elongated pulp horns Globular dentin – Reduced lamina dura – Increased radiolucency of alveolar bone  Nutritional Deficiencies VITAMIN K deficiency: (green leafy vegetables) Needed for coagulation factors 11, V, V11, 1X, X Oral: Gingival & post extraction bleeding VITAMIN B1 (thiamine) Deficiency: Clinical: Beriberi – Polyneuritis Muscle weakness – Cardiac failure Mental & growth retarded Oral: ? Rx Burning mouth syndrome ? Increased oral Ca  Nutritional Deficiencies VITAMIN B2 (riboflavin) Deficiency Skin: seborrhoeic dermatitis – Eye: corneal vascularization – Anemia (disturbance in folate utilization) Oral: (similar to folate deficiency) – Angular cheilitis (candida infection) – Glossitis & oral ulceration – Bluish discoloration of oral mucosa – Increased saliva (sialorrhea)  Nutritional Deficiencies VITAMIN B6 Deficiency: Participate in amino acid metabolism (decarboxylation, transamination, racemization) Clinical: Dermatitis & peripheral neuropathy Oral: – Angular cheilitis Glossitis – Stomatitis Bald tongue  Nutritional Deficiencies Biotin deficiency: (co-enzyme in carboxylation) Egg white binds biotin Clinical: Dermatitis Oral: ? Papillary atrophy (bald tongue) Nicotinic acid (niacin) Deficiency: Clinical: Pellagra – Dermatitis GI upset Neurologic disorder Oral: Generalized erythema of mucosa Bald tongue (papillary atrophy)  Nutritional Deficiencies Vitamin C (ascorbic acid) (fruits & vegetables) Potent reducing agent (anti-oxidant) Hydoxylation of proline (important for collagen) Clinical: Scurvy – Hemorrhage (due to capillary fragility) – Anemia Follicular keratosis of skin – Bone pain (infants) & fractures – Poor wound healing (weak scar formation) Oral: Gingivitis (swollen, bleeding, ulcerated) Alveolar bone loss Loose teeth  Progeria Autosomal recessive Clinical: – Dwarfism (height of 3 y o child) – Precocious aging (atrophic skin & loss of hair) – Death from CHD by age 10 – Squeaky voice – Parrot beak nose – Exophthalmos Oral: Hypoplastic mandible Delayed Eruption  Renal Disease Definition: Progressive destruction of kidney No excretion of urine or hormones Nephrotic syndrome: – Anorexia Edema of ankles – Weakness 4+ protein in urine End stage renal disease Azotomia = urea in blood Advanced renal disease Loss of 90% kidney function  still perform  Renal Disease Etiology: Acute renal failure – Ischemia Drugs – Trauma Septicemia – PROM Toxic agents Chronic renal failure – Abnormalities Nephrosclerosis – Systemic disease (diabetes, lupus) HBP – Chronic glomerulonephritis, pyelonephritis – Drugs  Common Systemic Manifestations of Renal Neuromuscular Disease Lethargy,mental slowness, weakness, lassitude Cardiovascular Hypertension, pericarditis, cardiomyopathy, CHF Dermatology Pruritis, easy bruising hyperpigmentation Hematologic Increased bleeding, lymphopenia, anemia (decreased erythropoietin) Metabolic Diabetes, lipid disorders Endocrine Hyperparathyroidism (GCT)  Common Test to Diagnose Renal Disease Glomerular filtration Rate (GFR) N = 120 cc/min < 10 c/min = renal failure Blood urea nitrogen (BUN) N < 20 mg/100 ml > 50 mg/100 ml  bleeding Creatinine level N < 1.5 mg/100 ml > 5 mg/100 ml  systemic problems Electrolytes Hyperkalemia & hypocalcemia  cardiac arrhythmia Radiographs Stones, kidney size & contour Ultrasonograph Tumors, cysts, obstruction  Treatment of Renal Disease Early stage Strict diet & electrolyte control Late stage Dialysis Hemodialysis: Metabolic waste removed by passing patient’s blood thru semipermiable membrane Blood is heparinized and returned to patient Arteriovernous fistula made for long term dialysis  Treatment of Renal Disease (cont) Periotioneal Dialysis Advanced cases Slower Abdominal periotoneum acts as filter Renal Transplant From relative (prefered) or cadarver Life time regimen of immuno-suppressive drugs Pharmacologic Management of Renal Disease Considerations Management Compromized Careful adjustment of dose excretion of & time sequence. Know drugs drug interactions & site of clearance Undergoing Avoid drugs not dialysed dialysis (consult with pharmacist) Drug nephrotoxicity Consult with pharmacist Pharmacologic Management of Renal Disease (cont) Antibiotics Avoid tetracycline  dangerous increase in BUN No streptomycin or polymyxin B Analgesics Avoid salicylates & NSAID  bleeding & fluid retention Dental Management of Patients With Renal Disease Thorough knowledge re renal disease: – History – Etiology – Extent of organ systems involved – Lab test & treatment modalities – Warning signs of infection (may be masked) – Prophylactic antibiotic coverage BEST TIME TO TREAT PATIENTS ON DIALYSIS IS THE DAY AFTER A DIALYSIS SESSION  Gastrointestinal Tract (GIT) Diseases Plummer-Vinson (Patterson-Kelly) Syndrome Clinical: Mainly post menopausal female Dysphagia: Predominant feature Thin diaphanous leukoplakic web across upper 1/3 esophagus Oral manifestations Iron deficiency anemia  “bald” painful tongue, angular cheilitis Oral leukoplakic lesions  Carcinoma Biopsy leukoplakic lesions  Inflammatory Bowel Disease Crohn’s Disease: Granulomatous lesions from mouth to anus Clinical presentations: Mostly young adults (peak in 6th decade) Mostly Ileo-caecal in site Signs/Symptoms: Abdominal pain Malaise Clubbing of fingers Fever Rectal bleeding, fissures, fistula & skin tags Weight loss  Crohn’s Disease (cont) Oral Manifestations: Recurrent oral aphthous ulcer (25%) Oral lesions may be first clinical manifestation or be only site of the disease Oral chronic inflammatory hyperplastic lesions with “cobblestone” appearance Increased caries (due to high sucrose intake) Medical Management: (improves oral lesions) Sulphasalazine, Steroids, Zinc & Copper Oral Management Good oral hygiene+Fluoride  Ulcerative Colitis Chronic inflammation of colon & rectum mainly Signs/Symptoms Rectal bleeding Weight loss Abdominal pain Oral Manifestations: Recurrent aphthous ulcers (4 – 20% ) Pyoderma gangrenosum-like lesions (irregular ulcers with purple rolled edges on a gray base) Pyostomatitis vegetans (deep fissured ulcers separated by papillary projections)  Peptic Ulcers Definition: ulcer penetrating thru muscularis mucosa in areas bathed with acid & pepsin Etiology: Helicobacteria pylori Signs/Symptoms: Gastric ulcer: pain aggravated by food Duodenal ulcer: pain relieved by food but recurs 1 hr after meal Medical Management: bland diet + milk, antacid, anticholinergics, carbenoxolone Dental Management: NO NSAID or STEROID  Human Immunodeficiency Virus Disease (HIVD) Introduction DHCW play important role in – overall care of HIV-infected individuals – resource to the community on HIV issues Incorporation of identified HIV-infected patients into a general dentistry setting is essential as the growing number of infected individuals cannot be accommodated by specialty clinic alone  HIVD & Acquired Immune Deficiency Syndrome (AIDS) Introduction (cont) Oral manifestations of HIV disease should be recognized by all DHCW Following established infection control guidelines, such as barrier techniques, disinfection & sterilization procedures have been shown to minimize the transmission of HIV & other infectious diseases in the dental clinic  HIVD/AIDS Legal Issues Anti-discrimination laws limits the discretion of DHCW to refuse treatment to patients with disabilities, including HIV infection. Under the Disabilities Act, dental offices are places of public accommodation, are are prohibited from refusing to treat patients solely due to their HIV status This prohibition applies to current patients as well as new patients.  HIVD/AIDS Legal Issues (cont) These laws correspond closely with the conduct required by the Principles of Ethics & Code of Professional Conduct of the Jamaica Dental Association, which specifies that patient referrals should be based on the treating DHCW’s inability to perform the required dental procedure. Under the principles a patient’s HIV status is not an appropriate basis for referral.  HIVD/AIDS Legal Issues (cont) The confidentiality of dental records containing HIV-related information is strongly protected by law. It is advisable to acquire a written release of HIV- related information The dentist is ultimately responsible for the conduct of staff, and will be held responsible for any release of information  HIVD/AIDS Epidemiology: End 0f 2002 Caribbean: Epidemic started late 70s, early 80s Adults & children living with HIVD: 440,000 Adults & children newly infected: 60,000 Adult prevalence 2.4% % HIV negative: 50% Main mode of transmission (adults): Heterosexual & Homosexual males  HIVD/AIDS Epidemiology (cont) Estimated adult & child deaths (2002): 42,000 Country Living Deaths Orphans (end 2001) (during 2001) Bahamas 6200 610 2900 Barbados 2000 I/D I/D Cuba 3200 120 1000 Dominican R 130,00 7800 33,000 Haiti 250,000 30,000 20,000 Jamaica 20,000 980 5100 Trinidad 17,000 1200 3600  HIVD/AIDS Pathogenesis HIV infection  immune dysregulation, dysfunction & deficiency Develop major opportunistic infections Develop autoimmune conditions & neoplasms High morbidity & mortality AIDS = end stage of HIVD T4-helper lymphocytes (CD4 cells) destroyed Median incubation period of HIVD, from initial infection to first signs of AIDS is 10 years  HIVD/AIDS HIV-related Information Past/present HIV Determine stage of disease related illness & influence treatment plan & care Past Lab results Indicate course of disease & influence long term goal of dental therapy Present Lab results Provide blood & HIV status & determine type of ongoing care MedicationsSide effects re oral cavity  HIVD/AIDS Current Diseases of Concern to DHCW Disease Concern __________________ TB Risk of infection Multiple drug resistant cases Hepatitis B Liver damage. Risk of contagion virus infection STD Potential contagious oral lesions. Systemic manifestations (heart, CNS) Mulluscum Highly infectious oral/skin contagiosum lesions  HIV Testing Enzyme-linked immunosorbent assay (ELISA) – Detects a general antibody response to HIV Western blot (WB) – Detects antibody response to specific HIV protein Polymerase chain reaction (PCR) – Detects HIV mRNA & DNA 95 % will be Ab + within 6 mths of exposure Abs may not show during first 3 mths  HIV Testing Procedures Must do pre- & post-test counseling Indications for HIV Testing of Dental Patients Clinical manifestations raise suspicion HIVD Post needlestick exposure protocol Involuntary testing of patients blood can be court ordered In order for one to be considered HIV +, 2 ELISA & 1 consecutive WB must be positive for anti- HIV  Pertinent HIVD Lab Tests & Values CD4 cell/mm3 Adults_____________________ > 600 Normal < 500 Initial immune suppression < 400 Opportunistic infections 200 – 400 Major opportunistic infections < 200 Severe immune suppression AIDS diagnosis < 100 Fatal opportunistic infections < 50 Very poor prognosis  Pertinent HIVD Lab Tests & Values CD4 count determine disease stage & influence appropriate dental treatment plan CD8 cell count N = 272 – 931. Suppressor cells. High numbers beneficial to patient. CD4:CD8 ratio: Low ratio indicates immune suppression p24 antigen: indicates active viral replication & suggest disease progression P24 antibody: indicates latent disease stage No need for prophylactic meds prior to dental treatment based solely on p24 or CD4 status.  Pertinent HIVD Lab Tests & Values Platelet count: – Thrombocytopenia (< 150,000 /mm3) present in 50 – 60% adults with AIDS – Dental treatment, including extractions, can be safely performed with platelet count > 60,000 ) WBC & Differential: – Leukopena (WBC < 4,500 cell/mm3) present in 40 – 60 % of patients with AIDS – Prophylactic antibiotics with neutrophil count < 500 cells/m3  Pertinent HIVD Lab Teasts & Values Hemoglobin: – Many HIV patients are anemic (Hb 7-10 g/dl ) – (Normal Hb: males 14-18; females 12-16) No contraindications for general dental procedures, including single extractions: – Bleeding time & coagulation values normal – Hb > 7.0 g/dl Avoid respiratory depressive drugs with Hb < 10g/dl  Pertinent HIVD Lab Tests & Values Prothrombin Time (PT) of 9 – 11 seconds Partial Thromboplastin Time of 28 – 38 seconds – Indicates no liver damage General dentistry, including extractions safe: – PT & PTT values 2x normal levels – Sufficient platelets (> 150,000/mm3)  Anti-Retroviral Drugs Name Indication Complications Nucleoside analogues (stops building process) (zidovudine, AZT) CD4 6 mos  chronic carrier state HBcAg – Non detectable in serum, only hepatic cells HBeAg – Appear same time as HBsAg – Seroconverts to anti-Hbe at peak of symptoms – Non-converts  chronic HBsAg carriers  HBV Antibodies Anti-HBs – Not detectable until HBsAg turns negative – Delay between disappearance of HBsAg & appearance of anti-HBs = “window” – Confers permanent immunity – Only Ab response from HBV vaccination – Principal component of HBIg – Long lived Ab – 5 – 10% of patients do not produce this Ab  HDV Antibodies Anti-HBc – Detected in serum shortly before onset of symptoms – Appears in all patients – Accurate marker of present & past infection – Only positive in “window period” – With positive HBsAg acute/chronic infection  HBV Antibodies Anti-Hbe – Appearance suggest infection & disease are waning – Appearance predicts probable recovery & pending clearance of Ant-HBs – Important in evaluating chronic HBV infection Serum positive for HBsAg & HBeAg is 30,000 more infectious than serum positive for HBsAg only