Principles of Internal Medicine PDF for Dental Students - SGS411T 2012

PRINCIPLES OF INTERNAL MEDICINE FOR DENTAL STUDENTS PROF.DR.M.SHERIF EL DEGWI DR.AHMED ABDEL HAKIM [SGS 411] Page 1  MSA PRINCIPLES OF INTERNAL MEDICINE FOR DENTAL STUDENTS PROF...

PRINCIPLES OF INTERNAL MEDICINE FOR DENTAL STUDENTS PROF.DR.M.SHERIF EL DEGWI DR.AHMED ABDEL HAKIM [SGS 411] Page 1  MSA PRINCIPLES OF INTERNAL MEDICINE FOR DENTAL STUDENTS PROF.DR.M.SHERIF EL DEGWI MD Cardiology, Fellowship of Texas Heart Institute Professor of Cardiology, Cairo University DR.AHMED ABDEL HAKIM ABDEL AAL Fellowship of Royal Colleges of Physicians (Edinburgh) Lecturer of Internal Medicine, MSA University Page 2 Contents Preface 5 Cardiovascular 8 I. Structures of the heart: 9 II. Circulation of blood through the heart : 12 III. Clinical manifestation of cardiac disorder: 13 Chest pain 14 Causes of chest pain : 14 Coronary heart disease 17 Angina 18 MYOCARDIAL INFARCTION (M.I) 24 HEART FAILURE 29 Hypertension 34 Rheumatic fever 43 INFECTIVE ENDOCARDITIS 48 SYNCOPE 52 ARRHYTHMIA 55 CHEST 58 Anatomy and function of the respiratory system: 59 Clinical Manifestation Of Lung Disease 60 CHEST DISEASE 64 Lung Diseases: 67 2.Airway diseases: 74 3.Interstitial lung Disease: 78 DISEASES OF THE PLEURA 78 Haematology 81 Blood components: 82 Functions of blood components: 83 Blood component disorders (Blood diseases): 83 Erythrocyte sedimentation rate (ESR): 84 Page 3 Anemia 85  Definition 85 Causes & types : 85 Hereditary types of anaemia : 88 Clinical Picture of anaemia : 90 Signs of Anaemia : 90 Haemostasis &Bleeding Disorders 92 HAEMOSTASIS AND THROMBOSIS: 92 I.THROMBOSIS: 92 II. Bleeding disorder : 97 Blood malignancies 102 Leukaemia 102 II. Lymphomas 103 Blood-borne diseases 104 Human immunodeficiency virus (HIV) 104 Common Oral Conditions associated with HIV: 105 Major manifestations of gastrointestinal diseases 109 PEPTIC ULCER 111 JAUNDICE 114 Liver disease 120 LIVER CIRRHOSIS 121 VIRAL HEPATITIS 125 5 Page 4 Preface Medicine is a broad science. This book is by no means conclusive of internal medicine. It is only hoped to introduce dental students to basic principles of internal medicine that would enable them to deal with dental patients with medical problems safely. Emergency and First Aid as medicine were given special attention since dentist are liable to face such conditions in their practice and should be able to manage. Furthermore, we also want to give a brief synopsis of common diseases facing doctors during their practical life. The discussion classes and clinical lectures will help students broaden their medical knowledge and detect common clinical signs of diseases. The information in this book is supported by illustrations that help deliver the message in a simple manner. We hope that at the end of this course students will know basic medical knowledge that helps them prevent the spread of infectious diseases that can be transmitted by dental procedures, for the patient’s ultimate safety and benefit. PROF.DR.M.SHERIF EL DEGWI MD Cardiology, Fellowship of Texas Heart Institute DR.AHMED ABDEL HAKIM ABDEL AAL Fellowship of Royal Colleges of Physicians (UK) Page 5 Acknowledgements All thanks and gratitude go to GOD, the most Beneficent & Merciful. First & foremost, I would like to thank my parents for their exquisite devotion & keen interest throughout my life, which helped me be who I am today. It is to them I dedicate this work. Words can never be enough to express my sincere appreciation to Professor Sherif El Degwi for his valuable guidance , continuous encouragement & endless support throughout my career. Dr. Ahmed Abdel Hakim Page 6  Dedication To Mahi My lovely niece whose picture had been in my mind all through the revision of this book. Prof. Dr. Sherif el Degwi Page 7  Cardiovascular system Objectives and Goals: The overall objectives of this topic are: 1. Supplying the basics of common cardiovascular diseases & their symptoms. 2. Introducing the students to the basic principles of Ischaemic heart disease, Heart failures, Hypertension, rheumatic fever & Infective Endocarditis. 3. Delivery of basic knowledge for cardiac emergencies (Cardio pulmonary resuscitation, syncope & arrhythmia). Page 8  Cardiovascular system I. Structures of the heart: Heart consists of Chambers, valves, conductive system& coronaries. a. Cardiac chambers: Consists of 2 Atria& 2 Ventricles made by cardiac muscles. Fig.1: Heart structures (After ADAMS) b. Valves: There are 4 valves : Mitral valve: Between left atrium& left ventricles. Tricuspid valve: Between right atrium& right ventricles. Aortic valve: Between left ventricles& aorta. Page 9  Pulmonary valve: Between right ventricles& pulmonary artery. c.Conductive system: Consists of i. Sinoatrial node. ii. Atrioventricular node. iii. Bundle of His (AV Bundle). iv. Right & Left Bundles and Purkinje fibres. Purkinje AV bundle Fig.2: Conductive system of the heart (Right) &Normal heart rhythm (left). fibres Normal cardiac rhythm results from electrical impulses that begin in a special group of cells that form the Sino atrial (SA) node, which is located in the right atrium.The sinus node acts as the heart's natural pacemaker. Impulses spread from the sinus node to the right and left atria Page 10 causing them to contract at the same time. The impulses then travel to the atrioventricular (AV) node to the Bundle of His (AV Bundle). From the AV Bundle, the impulses travel through conducting system (Located in the septum), this conducting system splits to form the right and left bundle branches which split to the purkinje fibers. d. Coronary arteries: It is originate from aorta &supply blood to the heart. There are left & Right coronaries which are divided to many branches. Fig.3: Normal coronary arteries. (After ADAMS) Page 11 II. Circulation of blood through the heart : In normal heart, The right side of the heart receives the systemic deoxygenated venous blood through superior & inferior vena cava and eject it in to pulmonary artery while the left side of the heart receives oxygenated pulmonary venous blood & eject it in to systemic arterial circulation. Pulmonary veins Aorta Pulmonary artery Inferior vena Fig.4: blood Circulation through the cava heart. (After ADAMS) Oxygenated blood. De oxygenated blood Page 12 III. Clinical manifestation of cardiac disorder: a. Pulmonary congestive symptoms: Dyspnoea, Orthopenia, cough& haemoptysis. b. Systemic congestive symptoms: Right hypochondrial discomfort, Dyspepsia, dependant oedema& ascites. c. Low cardiac out put symptoms: syncope, angina, easy fatigability &oliguria. d. Palpitation: Awareness of heart beat either due to disturbance in cardiac rhythm or rate. e. Chest pain: Is a pain or discomfort that is felt anywhere along the front of the body between the neck and upper abdomen. Any organ or tissue in the chest can be the source of chest pain, including heart, lungs, oesophagus, muscles, ribs, tendons, or nerves. Page 13  Chest pain Is a pain or discomfort that is felt anywhere along the front of the body between the neck and upper abdomen.  Alternative Names: Chest tightness or Chest discomfort. Causes of chest pain : chest pain Thoracic Extra-Thoracic Cardiac A Extra-Cardiac Neurological Abdominal Page 14 i. Thoracic causes: A. Cardiovascular causes: a. Angina: is heart-related chest pain. This pain occurs due to transient inadequate blood and oxygen supply to the heart. N.B:  Angina is called stable angina when chest pain begins at a predictable level of activity. (For example, when patient walk up a steep hill.)  However, if chest pain happens unexpectedly after light activity or occurs at rest (i.e.: chest pain change in frequency, Duration, severity& intensity) this is called unstable angina. This is more dangerous form of angina &need urgent referral to cardiologist. b. Myocardial infarction: is heart-related chest pain. This pain occurs due to cut off blood and oxygen supply to the heart. c. Pericarditis: is a disorder caused by inflammation of the pericardium (sac-like covering of the heart). d. Aortic dissection: is a condition in which there is bleeding into and along the wall of the aorta leading to splitting media layer. N.B: Arterial wall consists of 3 layers: Intima, Media & Adventitia Page 15  Fig.5: Aortic dissection (After ADAMS). B. Non Cardiac causes of chest pain include: a. Pulmonary embolism :see page 61 b. Pneumonia. see page 67 c. Pleurisy: inflammation of the pleura (membrane covering of the lungs). In these cases, the chest pain often worsens with deep breath or cough and usually feels sharp. d. Pneumothorax: presence of air in chest cavity. e. Musculoskeletal pain: Strain or inflammation of the muscles and tendons between the ribs. ii. Extra-thoracic causes: a.Anxiety and rapid breathing. b. Peptic ulcer & gastrooesophageal reflux: when acid from stomach backs up into the oesophagus lead to heartburn. c. Gallbladder Disease: Cholycystitis, gallstones. Page 16  Coronary heart disease  Definition : Coronary heart disease means decrease in blood supply to the heart ranging from mild impairment of coronary blood flow (Angina) to total coronary occlusion (Myocardial infarction). Coronary heart disease Ischaemic heart Myocardial infarction disease Stable Unstable angina angina N.B: Stable angina may progress to unstable angina while unstable angina is usually progress to myocardial infarction. Page 17  Angina  Definition: Is heart-related chest pain. This pain occurs due to transient inadequacy of blood and oxygen supply to the myocardium leads to imbalance between oxygen demand &supply.  Causes of angina: 1. Atherosclerotic coronary artery (99%): this occurs due to sub-intimal lipid deposition lead to plaque formation & narrowing of coronary lumen. Fig.6: Plaque structures (After Julian). Plaque: it is atherosclerotic lesion consists of cholesterol& smooth muscle cells with or without calcifications separated from coronary lumen by a thin fibrous cap. If this fibrous cap rupture lead to roughness of luminal wall lead to platelets deposition & thrombus formation. Page 18  Fig.7: Pathology of Ischaemic heart disease (After ADAMS). 2. Less common causes of angina include: a. Coronary artery spasm (also called Prinzmetal angina) b. Diseases of the heart valves(e.g. Aortic stenosis) c. Anaemia.  Incidence: There are approximately 400,000 new cases of stable angina diagnosed each year, according to the American Heart Association.  The risk factors for angina pectoris include: a) Non modifiable risk factors a. Male gender. b. Age: Increase in age increases the risk of heart disease. c. Family history of coronary heart disease. b) Modifiable risk factors Page 19  a. High serum cholesterol levels (in particular, high LDL and low HDL cholesterol). b. High blood pressure. c. Cigarette smoking. d. Diabetes e. Sedentary lifestyle. f. Obesity.  Types of Angina: 1. Stable angina. 2. Unstable angina. 1. Stable angina: Pathology: Plaque formation leads to narrowing of coronary lumen. Symptoms: Feeling of tightness, heavy pressure, squeezing or crushing chest pain that may spread to shoulder, arm, abdomen, jaw, neck, back, or other areas. Fig.8: distributions of chest pain (After ADAMS). Page 20  Pain occurs after activity, stress, or exertion Pain lasts 1 to 20 minutes Usually relieved with rest or nitroglycerin. Diagnose : ECG( may be normal). Exercise ECG: may show ECG changes. Coronary angiography. Treatment: The goals of treatment are to reduce symptoms and prevent complications. There are three primary forms of medication for stable angina: 1. Medications that improve long-term health include aspirin, clopidogrel (Plavix), and cholesterol-lowering drugs. 2. Medications that improve symptoms include nitrates. 3. Medications that do both include beta blockers and angiotensin-converting enzyme (ACE) inhibitors. Summary of the main medical treatment for ischaemic heart disease: A= Antiplatelets (Aspirin 83-300mg/day& Clopidogrel) &ACE inhibitor. B= Beta blockers (Atenalol, bisoprolol). C= Cholesterol lowering drugs (Statins). 4. Some patients may need intervention such as: Complications: 1. Unstable angina. 2. Heart attack (Myocardial infarction). 3. Arrhythmias. Page 21  4. Sudden cardiac death. Prevention: The best prevention for angina is to lower risk for coronary heart disease. Stop smoking. Weight Loss if the patient is overweight. Control blood pressure & diabetes.  Low cholesterol diet. 2. unstable angina: Pathology: It is occurs due to formation of non-occluding thrombus on rupture plaque. Symptoms: When chest pain has one of the following characters, it is considered as unstable angina. 1. Recent onset(less than 2 months) angina that is severs or frequent. 2. Accelerated angina that is becoming more sever & frequent longer or precipitated with less exertion than previously. 3. Angina at rest. Diagnose : ECG( may be normal). Exercise ECG: Contraindicated. Cardiac enzymes may be mildly elevated. Treatment: The goals of treatment are to prevent complications (M.I & Death). 1. Admission to coronary care unit. 2. Intravenous nitroglycerin, subcutaneous heparin, Oral Page 22  Aspirin, clopidogrel, Beta blocker, ACE inhibitors, Cholesterol lowering drugs. 3. Some patients may need intervention such as: a. Percutanueous transluminal Coronary Angioplasty (PTCA). b. Coronary artery bypass grafting (CABG). Dental management of patient with angina: 1. History (H/O): if last attack within last 2 weeks or there is unstable angina postponed appointment& Refer patient urgently to cardiologist. 2. Patient should come to the appointment fasting at least 4 hours. 3. Reduction of the fear& anxiety: Allow patient to express his faer, Pre medication with anxiolytic may be needed. 4. Give patient sublingual nitroglycerin at beginning of procedures. 5. Local anesthesia: Vasoconstrictor (Adrenaline) concentration 1/100,000 & not more & aspirate &inject slowly. 6. Treatment procedures: Painless & a traumatic procedures as possible& avoid vasopressor in gingival packing material. 7. If patient develop postural hypotension: Change chair position to get the patient head down. 8. If the attack developed: Stop dental treatment, give patient sublingual nitroglycerin tablet& if pain relived within 5 min you can continue the treatment. If pain does not relived within 5 min give another S.L nitroglycerin, terminate dental treatment & refer him to nearest hospital. Page 23  MYOCARDIAL INFARCTION (M.I)  Definition: Myocardial infarction is the term applied to the myocardial necrosis secondary to acute prolonged interruption of the coronary blood supply.  Pathology: Total occlusion of one or more of the coronary arteries by occluding thrombus.  Symptoms:  Crushing chest pain that may spread to shoulder, arm, jaw, neck, back, or other areas.  Pain occurs at rest.  Typically lasts longer than 20 min  The pain is not fully relieved by rest or Incidence: Fig.9: chest pain (After Macleod) nitroglycerine.  May associated with sweating& It is estimated that approximately 1 million patients in USA visit Vomiting. the hospital each year with a heart attack. Heart attacks account for 1 out of every 5 deaths. It is a major cause of sudden death in adults. Page 24  Risk factors: As in angina.  Diagnosis: a. Symptoms: chest pain (see above) b. Electrocardiogram(ECG) : Show ST elevation which may delayed for few hours. Fig.10: Comparison between ECG of acute M.I (Left) &Normal ECG (Right). b. Serum cardiac Enzymes:[e.g Creatine phosphokinase (CK)] it is an enzyme presents normally inside cardiac myocytes, released to the serum when cardiac muscle injury occur. CK raises within4 - 6 hours of infarction. c. Serum Troponin I &TroponinT (proteins involved in muscle contraction ): present normally inside cardiac myocytes, released to the serum when cardiac muscle injury occur. Elevated within3- 6 hour of infarction.  Treatment: The goals of treatment are to reperfuse the occluded coronary, to reduce the demands on the heart so that it can heal, and to prevent complications. Page 25 a. Admit the patient to coronary care unit. b. Give oral 300 mg aspirin, Clopidogrel & Sublingual nitrate. c. Oxygen by mask. d. Insert intravenous (I.V) line (e.g cannula). e. Give Pain killer (Intravenous Morphine sulphate). f. Intravenous nitrate. g. Consider Thrombolytic therapy(Streptokinase{STK}1,5 million unit over 1 hour I.V) within 12 hours of the myocardial infarction.(Most benefit if STK given in the first 6 hr). h. Other medication: Heparin, Beta blocker, Angiotensine converting enzyme (ACE) inhibitor. i. SURGERY AND OTHER PROCEDURES Emergency coronary angioplasty (procedure in which a balloon is used to open narrowed or blocked coronary arteries). This procedure used for coronary reperfusion instead of thrombolytic therapy if facilities for angioplasty are available, or in cases where thrombolytics should not be used or failed to reprefuse occluded coronary. A device called a stent is often inserted into the artery during angioplasty, to help ensure that the newly opened coronary artery remains open after surgery. Emergency coronary artery Page 26  bypass surgery (CABG) may be required in some cases. Fig.11: coronary angioplasty with stenting (After www.dmcardiologie.com).  Complications: 1. Arrhythmias such as ventricular tachycardia, ventricular fibrillation, heart block. 2. Congestive heart failure. 3. Cardiogenic shock (the Myocardium is damaged enough that it is unable to supply sufficient blood to the body). 4. Pericarditis. Page 27 Dental management of patients with myocardial infarction:  No routine dental care at least 3 months after infarction.  Do not do dental procedure for patient who has post infarction angina, unless emergency and take permission from cardiologist.  Appointment: better to be in the morning with the patient fasting, appointment better to be short to avoid patient fatigue.  Reduction of anxiety: diazepam 5mg oral 30 min before procedure.  Local anaesthesia: Epinephrine ( vasoconstrictor) should be at concentration 1/100,000 or less and only give carpule per-visit.  Treatment procedures: As painless and atraumatic procedures as possible and avoid vasopressor in gingival packing material.  If the chest pain developed: Stop dental treatment, give patient sublingual nitroglycerin tablet and if pain is relieved within 5 min. you can continue the treatment.  If pain is not relieved within 5 min give another S.L nitroglycerin, terminate dental treatment and refer him/her to nearest hospital. Page 28  HEART FAILURE  Definition: It is a condition where the heart cannot pump an adequate supply of blood to meet the metabolic needs of the body.  Types: Fig.12: Normal heart structures & circulation (After ADAMS). As the heart's pumping action is lost, blood may back up into other areas of the body, including:  The lungs (In left-sided heart failure).  The liver, the gastrointestinal tract and extremities (In right-sided heart failure).  The lungs, liver, GIT& extremities i.e. failure of both sides of the heart (Congestive heart failure). Page 29 I. Left sided heart failure: Causes : 1-valve disease (rheumatic or congenital) as: Aortic stenosis (Pressure overload), aortic & mitral regurgitation (volume overload). 2-Hypertension: causing pressure overload and left ventricular hypertrophy. 3-Myocardial disease: a) Myocardial infarction causing left ventricular wall necrosis. Necrotic areas are not contracting area (akinetic). b) Viral or Rheumatic Myocarditis. c) Cardiomyopathy: of unknown etiology causing weakness and hypocontractility of myocardium. Clinical Picture: 1. Dyspnoea: uncomfortable awareness of breathing. 2. Orthopnoea: Lying down increases venous return to the heart and provokes dyspnoea. 3. Paroxysmal nocturnal dyspnoea: In patients with sever heart failure, fluid shifts from interstitial tissues to circulation within 1-2 hrs after sleep causing pulmonary congestion. Page 30  Fig.13: Orthopnoea due to pulmonary congestion as x-ray shows. Fig14: Paroxysmal nocturnal dyspnoea (After McLeod) 4. Acute pulmonary edema: occurs due to sudden rise of pressure in left side of the heart, pulmonary veins and pulmonary capillaries. When hydrostatic pressure of Page 31  pulmonary capillaries exceeds oncotic (osmotic) plasma pressure, fluid moves from capillaries into alveoli. The patient becomes distressed, sweaty, cyanosed and coughs a frothy pink (blood-stained) sputum. 5. Low cardiac output symptoms causing poor perfusion of skeletal muscles leading to fatigue, of skin causing cold extremities, and peripheral cyanosis, of kidney causing oligouria, and brain causing headache. П – Right sided heart failure: Causes: 1. Cor pulmonale: is Rt sided heart failure due to chronic lung disease causing pulmonary hypertension. 2. Secondary to left sided heart failure Lt. sided heart failures leads to chronic Lt. atrial pressure elevation, pulmonary hypertension, followed by Rt sided heart failure (congestive heart failure). 3. Pulmonary embolism from venous thrombosis of lower limb. 4. Congenital pulmonary valve stenosis. 5. Myocardial diseases: myocardial infarction of right ventricle. Page 32  Clinical Picture: 1- Congested neck veins. 2-Enlarged, congested , painful, tender liver. 3- Lower limb oedema & later ascites occurs. Fig.15: Lower limb oedema (After ADAMS).  Principles of heart failure treatment:  Non medical treatment: Decrease salt, water & NSAIDs intake.  Medical treatment: 1. Treatment to improve acute symptoms (Acute pulmonary oedema): IV Morphine, IV Frusemide (diuretics), Nitrate infusion if blood pressure is acceptable, Dobutamine infusion (increase contractility in sever cases). 2.Treatment to decrease recurrence of symptoms& improves long term out come: ACE inhibitor, small dose Spironolactone (potassium sparing diuretics), small dose beta blocker, Digoxin (to increase contractility). Page 33  Hypertension  Definition: Hypertension means high blood pressure consistently over 139mmHg (Systole) &/or consistently over 89 mmHg (Diastole). Fig.16: Pressure of the blood on arterial wall (After ADAMS) Figure 1 N.B:  Normal B.P = ≤120/80 mmHg.  Pre-hypertension if B.P between (120/80 -139/89mmHg).  Systolic blood pressure is the "top" number of blood pressure measurement, which represents the pressure generated when the heart contract.  Diastolic blood pressure is the "bottom" number of blood pressure measurement, which represents the pressure due to vascular resistance while the heart in diastole (Relaxed). Page 34  Types of hypertension: A. Essential hypertension: has no identifiable cause. It may be caused by genetics or environmental factors. B. Secondary" hypertension: is high blood pressure caused by underlying disease. These diseases may include: Drugs: Non steroidal anti-inflammatory drugs(NSAIDs) ,Steroids, Sympathomimetics (Epinephrine) ,oral contraceptives. Endocrinological: Cushing disease (Hypercortosalism), Hyper& Hypothyroidism, Acromegally ( Growth hormone Secretion). Kidney disorders. Cardiovascular causes: Coarctation of the aorta. Fig.17: Coarctation of the aorta (After ADAMS)  Tumors : Phaeochromocytoma (Tumor from cells secreting Catecholamines, this tumor most commonly arise from adrenal medulla). Catecholamines: Are substances leading to vasoconstriction (e.g: Dopamine, Adrenalin…) Page 35  Risk factors: a. Family history of hypertension. b. Advancing age. c. Smoking. d. High salt intake. e. Stress. f. Over weight. g. Hypercholesterolaemia.  Symptoms: Usually, no symptoms are present. Occasionally patient may experience: a. Epistaxis (i.e. nosebleeds). b. Mild headache (Rare). c. Tiredness. d. Chest pain (crushing chest pain). e. Heart failure. f. Blurred vision. g. Confusion &Convulsion. N.B: Presence of Hypertensive encephalopathy (sever headache, Confusion, convulsion), chest pain& shortness of breath is a medical emergency need urgent admission to the hospital. Page 36  Diagnosis: Hypertension may be suspected when the blood pressure is high at any single measurement. It is confirmed when blood pressure constantly elevated over 1 4 0 systolic or 9 0 mmHg diastolic.  Complications: a. Cerebrovascular Stroke. b. Retinopathy (Retinal damage). c. Cardiovascular complications: Ischaemic heart disease, Congestive heart failure. d. Nephropathy (kidney damage). Retinal damage Fig.18: Hypertension complications (After ADAMS) Page 37   Treatment: The goal of treatment is to decrease risk of complications There is medical & non-medical treatment. Fig.19: Hypertension treatment (After ADAMS) The non medical treatment is :  Lose weight if you are overweight. Excess weight adds to strain on the heart. In some cases, weight loss may be the only treatment needed.  Exercise. Page 38   Adjust the diet as needed. Decrease fat and sodium -- salt, baking soda all contain sodium. Increase fruits, vegetables, and fiber. The medical treatment may include: Diuretics, beta-blockers, calcium channel blockers, angiotensin- converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or alpha blockers. Drugs Example Side effects Diuretics Thiazide & Hypokalaemia ,Hyperuracemia( uric loop diuretics acid). Beta- Atenalol, Bradycardia( heart rate), Bronchial blockers propronalol asthma Calcium Nifedipin Lower limb oedema. channel blockers ACE Captopril Dry cough, Hyperkalemia. inhibitors Page 39 The choice of antihypertensive drugs depend on the patients age as well as if he is suffering from an ischaemic heart diseases or diabetes i.e. the Beta blocker will be the first choice for hypertension treatment if the patient has ischaemic heart diseases. The next Algorism shows the choice of antihypertensive drug depends on age group. Algorism: Treatment of newly diagnosed Hypertension according NICE (National Institute for Health and Clinical Excellence) Clinical guideline (Updated Feb 2006). Page 40  Measurement of blood pressure: The cuff is wrapped around your upper arm and inflated to stop the flow of blood in brachial artery. Fig.20 a: blood pressure measurement (After ADAMS) As the cuff is slowly deflated, Auscultate with stethoscope over brachial artery to listen to the blood pumping through the artery. The first pumping sound is recorded as the systolic pressure, and the last sound is the diastolic pressure. Fig.20 b: blood pressure measurement (After ADAMS) Page 41  Potential problems that may arise during dental treatment of uncontrolled hypertensive patients:  Excessive bleeding may occur especially if blood pressure is significantly elevated.  Cerebral vascular accident or myocardial infarction due to excessive use of vasopressor with local anaesthesia in patient with uncontrolled hypertension. Dental management of patient with hypertension:  Blood pressure recordings should be taken for the entire patient in the first dental visit.  Blood pressure recordings should be taken every dental visit for patients who have hypertension.  If diastolic blood pressure is more than 110 mmHg, refer patient for medical care, do only the emergency treatment.  Patient should receive his antihypertensive medications at the day of the dental appointment.  Local anaesthesia: The Vasopressor (Adrenaline) concentration 1/100000 and not more.  Three carpules /visit & not more. Page 42  Rheumatic fever It is a non suppurative acute inflammation occurs after tonsillopharyngeal infection with group A streptococcai affecting connective tissue (especially those of the heart, joints, brain or skin)  Age: Commonly occurs between the ages of 5 - 15 years.  Etiology: It is an autoimmune (cross reactivity) with a group A beta hemolytic streptococcal pharyngitis or tonsillitis. The group A streptococcai are antigenic, and produce antibodies which mediate inflammation in various organs. Autoimmune: Means that immune system destroys normal body tissues.  Clinical Picture: 1-Migratory arthritis: affecting big joints causing red, warm, swollen, tender joint with limitation of movement. Arthritis is fleeting and leaves the joints normal Page 43  Fig.21: Arthritis as major symptoms of rheumatic fever (After ADAMS) 2-Carditis: It is pancarditis i.e. involves the three layers of the heart (Pericarditis, Myocarditis& Endocarditis).  Pericarditis: lead to chest pain.  Myocarditis: causing tachycardia and heart failure.  Endocarditis: causing valve damage Fig.22: Diagrammatic illustration of Pericarditis & Myocarditis (After ADAMS). Page 44  3- Chorea: Involuntary movements of hands, feet, face. 4- Subcutaneous nodules over bony areas. They are firm and painless. 5-Erythema marginatum: Red macules with pale center (red margins). Other symptom: Fever, Arthralgia (only pain around the joints), anemia, Epistaxis.  Investigations: 1. Raised E.S.R and positive C reactive protein (CRP).. 2. Leucocytosis. 3. Raised serum antistreptolysin O antibody titer(ASOT) above 200 units. 4. ECG. 5. Echocardiography. N.B:Throat swab culture for group A- β hemolytic streptococci usually shows no growth.  Diagnosis: For diagnosis, there should be at least 2 major criteria, or one major with 2 minor criteria in presence of elevated ASOT. Page 45  Major criteria Minor criteria 1. Migratory arthritis. 1. Fever. 2. Carditis. 2. Arthralgia. 3. Chorea. 3. High ESR or CRP. 4. Subcutaneeous 4. Prolonged PR interval in nodules ECG. 5. Erythema marginatum.  Complications: 1. Permanent valvular damage =chronic rheumatic heart disease: Any of cardiac valves can be permanently damaged leading to either regurge or stenosis or both regurge & stenosis to gather. The most common valve affected is mitral valves then aortic. Page 46  2. Heart failure: either due to Myocarditis (early) or due to sever long standing valvular lesion (Late complication).  Treatment:  Bed rest and supportive therapy.  Treat arthritis mainly by Aspirin.  In Carditis, Prednisone is used  Prophylaxis:* The aim is to eradicate streptococcal infection and prevent recurrence. 1- Primary prophylaxis* to prevent attack by proper antibiotic treatment of tonsillitis. Oral phenoxymethyl penicillin 500 mg 12 hourly for 10 days is given. 2- Secondary prophylaxis* to prevent recurrence after first attack by giving long acting Benzathine penicillin G 1.2 Million units I.M every 3 weeks.Erythromycin is used if patient is penicillin sensitive. * Prophylaxis: is a measure taken to maintain health and prevent the spread of disease. *1ry prophylaxis is a measure taken to prevent disease before occurrence. *2ry prophylaxis prevents recurrence of the disease. Page 47  INFECTIVE ENDOCARDITIS  Definition: It is bacterial or fungal infection of the endocardium involving the valves and adjacent structures, usually occurring over abnormal valve affected with congenital heart disease or other diseases. Fig.23: Vegetations over the mitral valves (After Mayo foundation)  Etiology: Bacteria or fungi enter the blood & attacks the heart.  Streptococcus Viridans, which are normal commensals in mouth and upper respiratory tract, can enter blood after dental cleaning, extraction or tonsillectomy. Page 48   Staphylococcus aureus enters the blood in drug abusers, or through I.V. catheters. N.B: Patients with congenital heart disease or prosthetic valve are vulnerable to colonization by these bacteria causing vegetations, which are formed of platelets, fibrin, and organisms.  Clinical picture:  Fever, pallor, and weight loss.  Damage of cardiac valves leading to aggravation of old valvular lesion & precipitation of heart failure.  Mucocutaneous lesions: subconjunctival , soft palate petechiae, splinter hemorrhages (hemorrhages in the nail beds), painful subcutaneous nodules (tender nodules are located in the terminal phalanges of the fingers and toes.  Systemic embolization of vegetations causing peripheral arterial embolism, in cerebral arteries (hemiplegia),renal artery (renal infarction and hematuria),lower limb arteries(ischemia, gangrene).  Splenomegaly.  Finger clubbing. Page 49  Causes of finger clubbing: 1. C.V disease: Cyanotic heart disease, IEC. 2. Lung Diseases: Bronchogenic carcinoma, suppurative lung diseases, lung fibrosis (cryptogenic) Fig.24: Finger clubbing (After ADAMS) 3. GIT causes: Malabsorption, liver cirrhosis.  Diagnosis:  Blood culture.  Echocardiography (is a sonography of the heart. Also known as a cardiac ultrasound). It can provide a helpful information, including the size and shape of the heart, its pumping capacity and the location and extent of any damage to its tissues. It is especially useful for assessing diseases of the heart valves. It not only allows doctors to evaluate the heart valves, but it can detect abnormalities in the pattern of blood flow, such as the backward flow of blood through partly closed heart valves, known as regurgitation.  Anemia, leucocytosis, thrombocytopenia may be present  Prophylaxis: I. Indications : According to American heart association, the only patients should take antibiotics before dental procedures are those: a. With artificial heart valves. b. Who have already had infective endocarditis. Page 50 c. Whose serious congenital heart defects have been incompletely repaired or have not been repaired. d. Who have a congenital heart defect that that was completely repaired using artificial material or a device for six months after the procedure. e. Whose heart defect was repaired but who have some of a defect near a patch or device made of artificial material. f. Who have had a heart transplant but has a defect in a heart valve. Those who have taken antibiotics in the past but no longer need to (based on the updated guidelines )include: 1. People With mitral valve prolapsed. 2. Rheumatic heart disease (Still receiving prophylaxis in Egypt). 3. Bicuspid valve disease. 4. Narrowing of the aortic valve that has calcium deposits. 5. Some kinds of congenital heart conditions, These include ventricular septal defect, atrial septal defect and hypertrophic cardiomyopathy. 6. The guidelines also do not recommend preventive antibiotics for common procedures to the gastrointestinal tract (stomach and intestines) or those on the urinary tract – even for patients at high risk of infective endocarditis. II. Antibiotic prophylaxis regimen:  Amoxicillin 2 gm 1 hour before procedure is to be taken orally. Or 2 gm Ampicillin iv within 30 min before procedure. Page 51   In patients allergic to penicillin, Clindamycin 600 mg 1 hour orally before procedure is used. SYNCOPE  Definition: It is a transient loss of consciousness secondary to decrease in cerebral perfusion ,recovery is spontaneous without neurological deficits.  Causes: 1. Neurocardiogenic Syncope: as Vasovagal Syncope: Precipitated by fright or anxiety which leads to vasodilatation leading to venous pooling and decreased venous return to the heart. Recovery occurs within few seconds, especially if the patient lies down. Fig.25: shock position (After ADAMS) Page 52  2. Cardiovascular Syncope: Arrhythmias. Obstruction: as aortic stenosis, pulmonary embolism. 3. Orthostatic Syncope: (Postural Hypotension) It is due to inadequate reflex vasoconstriction on standing from a lying or sitting position leading to a drop in BP and decreased cerebral perfusion. 4. Neuropsychiatric syncope.  Treatment: Immediate treatment for someone who has fainted includes: Air Circulation Breathing Way Page 53 1. Checking the person's airway and breathing. 2. Checking Blood pressure. 3. Loosening tight clothing around the neck. 4. Keeping the affected person lying down for at least 10 minutes, preferably in a cool and quiet space & elevating the feet above the level of the heart. 5. If vomiting has occurred, turning the person onto one side to prevent choking & aspiration. Fig.26: Shock position to prevent aspirations (After ADAMS) 6. Refer the patient to the nearest hospital. Page 54  ARRHYTHMIA  Definition: An arrhythmia is any disorder of heart rate or rhythm. Normal heart rate = 60 - 99 beat/min. Normal heart rhythm = Sinus rhythm (impulse generated from SA node). Fig.27: Normal heart rhythm  Types: i. Disorder of the rate: 1. Sinus bradycardia: Heart rate less than 60 b/min. It is usually asymptomatic unless being very slow, it could be due to many causes but the most common causes are physiological &drug induced. 2. Sinus Tachycardia: Pulse rate > 100 b/min. It is caused by fever, exercise, emotions, anemia, thyrotoxicosis & pregnancy. Page 55 ii. Disorder of the rhythm : 1. Ectopic beats: (it is either from atria or ventricles, if the ventricular ectopic beats occurs alternate with normal sinus beat this called Bigeminy. 2. Atrial fibrillation: This arrhythmia characterized by rapid irregular heart rate due to multiple ectopic foci in the atria leading to contraction of the atria in a very disorganized and abnormal manner. Causes of atrial fibrillation: Idiopathic. Mitral stenosis. Thyrotoxicosis. Ischemic heart disease. Hypertension. Treatment of atrial fibrillation:  Anticoagulant with warfarin  Heart rate control. Fig.28: Atrial fibrillation Any patient presents with arrhythmia leads to instability of vital signs, refer patients urgently to nearest hospital. N.B: The heart rate in atrial fibrillations should be counted over the cardiac apex by stethoscope not from radial pulse, why? Page 56 Learning out come of cardiology study: By the end of this course the students should: 1. Recognize & understand symptoms & signs of heart diseases. 2. Enumerate & avoid causes that can lead to hypertension & ischemic heart diseases. 3. Enumerate cardiac lesions that predispose to infective endocarditis & ways of preventions. 4. Gain familiarity with safe dental procedures for cardiac patients especially that have ischemic, rheumatic heart disease or receiving anticoagulant. 5. Discuss shock & First Aid for cardiac emergencies. Page 57  CHEST Objectives and Goals: The overall objectives of this topic are: 1. Supplying the basics of common chest diseases & their symptoms. 2. Introducing the students to the basics principles of concepts of droplet infections as causes of common chest diseases. 3. Delivery of basic knowledge for chest diseases that can complicate dental procedures e.g. aspiration pneumonia. Page 58  CHEST Anatomy and function of the respiratory system: The respiratory system is divided into the upper and lower respiratory tracts. Upper respiratory tract : The major structures of the upper respiratory tract include the nose , pharynx , larynx and trachea. Fig. 29 : Functional anatomy of the lower respiratory tract (After ADAM) Lower respiratory tract: The major structures of the lower respiratory tract include the bronchi, bronchioles, and alveoli. The main functions of respiratory system are to supply oxygen (O2) & removal carbon dioxide as needed by the metabolic demands of the body. Other functions include regulation of acid base balance …etc. Page 59 Clinical Manifestation Of Lung Disease 1. Cough & Expectoration: It is an explosive expiration. Types: Dry Cough Productive cough with expectoration of sputum. 2. Haemoptysis: It is coughing up blood from the lower respiratory tract. Causes: A. Respiratory causes: Respiratory infections. Tumors. Pulmonary infarction. Chest trauma. B. Cardiac causes: That lead to pulmonary congestion causing capillary rupture e.g. Mitral stenosis, LVF….etc C. General causes: Bleeding disorders. Other differential diagnosis of bloody spitting: is upper respiratory tract bleeding. Page 60 3. Chest Pain: Causes: Discussed in cardiology. 4. Dyspnea: It is difficulty in breathing (awareness of breathing). Causes: A. Respiratory causes: a. Upper airway obstruction e.g. Stridors. b. Lower airway obstruction (Bronchial Asthma). c. Pulmonary embolism:is a blockage of the pulmonary artery or one of its branches by circulating insoluble material, usually occurring when a venous thrombus (blood clot from a vein) becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs. B. Cardiovascular causes: Heart failure, mitral stenosis (leads to pulmonary congestion). C. General causes: Hysterical dyspnea (Common), hysterical personality, sighing. Anaemia. Page 61  Fig.30: Diagrammatic illustration of systemic & pulmonary circulations, to demonstrate the mechanism of cardiac dyspnoea via pulmonary capillary congestion (After ADAM) 3 5. Wheezes: It is musical sound due to partial narrowing of the bronchi e.g. in bronchial asthma. 6. Cyanosis: it is bluish discoloration of skin &mucus membrane. Types:  Peripheral cyanosis: seen in fingers ,toes & tip of nose. It is caused by blood stagnation (blue discoloration due to excessive oxygen(O2) extraction& accumulation of deoxygenated Hb, this is can occur in peripheral vascular constriction either Page 62 physiological (e.g. Cold weather) or pathological (Peripheral vascular disease). Fig.31: Peripheral cyanosis (After ADAM)  Central cyanosis: seen in Mucus membrane (tong, lips) & skin (finger, toes & nose tip). Causes of central cyanosis: Congenital heart diseases leading to shunting of some deoxygenated blood from right side to left side of the heart by passing oxygenation by the lung. Advanced lung diseases. Massive pulmonary embolism. Page 63  CHEST DISEASE Upper respiratory Lower respiratory tract diseases tract diseases i.e. below the trachea Page 64  Upper respiratory tract infection. Common cold (rhinitis), influenza, laryngitis (inflammation of the voice box), pharyngitis (sore throat), sinusitis, tonsillitis, and croup ( in children ). Page 65  Lower respiratory tract disease Lung diseases Pleural &Chest wall diseases Lung parenchyma Air way disease 1. Pleural effusion. 2. Empyema. Infection Interstitial 3. pneumothorax. lung 4. Neuro muscular disease diseases. Pneumonia. Bronchial asthma. Tuberculosis COAD. Page 66 Lung Diseases: 1. Lung infections: a.Non suppurative lung infection: Acute: streptococcal pneumonia, aspiration pneumonia, acute bronchitis. Chronic: tuberchelosis. b. Suppurative lung infection: Acute: Staph pneumonia, lung abscess. Chronic : Bronchiactesis. PNEUMONIA  Definition: Acute inflammation of lung parenchyma with accumulation of neutrophils, red cells, and fibrin in alveoli leading to lung consolidation (the lung becomes solid instead of its spongy character).  Organisms: a. Bacterial: streptococcal pneumonia, less common: Page 67  Homophilus influenza, staph aureus and Gm - ve bacteria(e.g Kellebsila) in hospitalized& immunocompromized patients. b. Viral. c. Rare causes: (less than 10%).  Symptoms: 1. Sudden onset of high fever. 2. Chills and myalgia. 3. Cough. 4. Pleuritic chest pain.  Complications: Fig.32: chest x-ray show bronchopneumonia 1. Lung abscess. 2. Pleural effusion and/or empyema. 3. Respiratory failure. Anatomical Classification of pneumonia :  Localized lobar pneumonia affecting one lobe of the lung.  Diffuse pneumonia, affecting more than one lobe (patchy and bilateral) called bronchopneumonia.  Pneumonia involved right lower lobe is usually due to aspiration pneumonia. Aspiration pneumonia: Aspiration of foreign body or gastric content (as HCL) complicating vomiting especially during Page 68  anesthesia or coma. ASPIRATION PNEUMONIA  Definition: Inflammations of the lung due to inhalations of the foreign body or gastric content (as HCL). Fig.33: Normal vocal cords Fig.34: Anatomy of upper air way (After www. homepages. cae.wisc.edu ) (After www.humanillnesses.com) Causes: 1. Loss of protective cough reflex with inhalation of septic material or vomitus as in coma or anesthesia (e.g. in dental, nose, throat surgery). 2. Paralysis of palatal and pharyngeal muscles Fig.35: Mechanism of aspiration (After ADAM) or vocal cord palsy. Page 69  3. In elderly and children because of impaired cough reflex. Complications of foreign Body aspiration: a. In larynx: impaction occurs &if it is large causing suffocation and stridor (difficult inspiration with cyanosis). b. It may be inhaled down into a right bronchus leading to bronchial obstruction (mainly right as it is wider and continuous with the trachea) causing retention of secretions followed by infection leading to pneumonia of right lower lobe , lobe collapsed or lung abscess. Relief of laryngeal obstruction caused by foreign body is life saving: i. Non invasive methods: Pediateric: Turn the patient head down tap vigorously over his back. Adult: Sudden forceful compression of upper abdomen (Heimlich maneuver). ii. Invasive methods:(when previous methods failed) Removal of foreign body by laryngoscopy. Urgent tracheostomy. N.B: Foreign body in the bronchus can be removed by bronchoscopy. Page 70  TUBERCULOSIS It is a contagious bacterial infection caused by Mycobacterium tuberculosis (TB). is a disease that has increased in prevalence in recent years, largely caused by the immunocompromised HIV population, in the malnourished.  Mode of infection: A. Pulmonary TB: by inhaling infected sputum, once the organism is inhaled; it reaches the pulmonary parenchyma where it is deposited. Fig.36 Transmission of pulmonary T.B. B. Bovine (in cattle) TB: It spreads by intake of unboiled milk causing intestinal T.B. and ascites. PULMONARY TUBERCULOSIS Spread of pulmonary TB: Local :To other lung tissue. Page 71  Haematological: To other organs like bones, meninges, genitourinary system and joints are affected by blood spread. Lymphatic spread: To pleura.  Pathogenesis: a. Primary T.B: Most primary infections are subclinical. Inhaled T.B bacilli 1ry lung lesion+ enlarged hailer lymph nodes. 90% healed with dormant bacilli 1 ry Lung lesion 10% spread to the other organ b. Post primary disease: occurs in adults when exposed to a sputum positive tuberculous patient or when immunity decreases leading to reactivation of primary disease. c. Miliary T.B: Uniform multiple infiltration of the whole lung, with blood spread to many other organs.  Diagnosis: Sputum staining &culture for TB bacilli. Tuberculin test. PCR (Polymerase Chain Reaction). Plain X-ray chest may show fibrosis or apical consolidation and cavitations. Page 72  Dental management for patient with T.B:  The patient with T.B is unlikely to be a great risk to dental staff unless the patient has an active pulmonary type with tuberculous bacilli presents in his sputum (Open TB) in which case dental treatment is better deferred until control has been achieved.  If delayed dental treatment is not possible aerosols should be reduced to a minimum and it may be useful to carry out treatment under rubber dam, Masks and spectacles are mandatory for all personnel.  Treatment and prevention:  Isoniazid and Rifampicin are the keystones of treatment, but because of increasing resistance to them, Pyrazinamide and either Streptomycin or Ethambutol HCL are added to regimens. If the patient is unable to take Pyrazinamide, a nine- month regimen of Isoniazid and Rifampicin is recommended.  BCG, or bacille Calmette-Guérin, is a vaccine against tuberculosis. The BCG vaccine is prepared from a weakened strain of Mycobacterium bovis. BCG is used in many countries with a high prevalence of TB to prevent tuberculous meningitis and miliary disease (aggressive form of tuberculosis that is characterized by a wide dissemination into the human body). Page 73 2.Airway diseases: BRONCHIAL ASTHMA It is a chronic inflammatory disease of airways leads to reversible airflow (Bronchiole) obstruction. Fig.37: Bronchial asthma  Classification:  Extrinsic asthma with a definite external cause. Onset is in childhood & frequently associated with other atopic disease e.g. rhinitis and dermatitis.  Intrinsic asthma with no causative agent. Onset usually in middle age. Page 74   Triggers of asthmatic attacks: 1. Allergens. 2. Irritants: Volatile gases. 3. Air pollution 4. Respiratory infections especially viral. 5. Cold air and exercise (thermal changes). 6. Drugs e.g. Beta-blockers, Aspirin.  Clinical Picture: Recurrent attacks of: 1. Dyspnea and wheezing which become worse during early morning. 2. Cough. Treatment: Decrease air way inflammation: Inhaled Corticosteroids (not in sever or life threatening asthma) or Systemic corticosteroids (in acute or chronic severe asthma). Side effects of inhaler corticosteroid: 1. Oral candidiasis. 2. Hoarsenes of the voice. Brochodilators: Beta 2 agonists inhaler, Ipratropium bromide inhaler (Anticholinergic). Methylxanthines as Theophylline. Fig.38: Inhalers used in bronchial asthma treatment Page 75  CHRONIC OBSTRUCTIVE AIRWAY DISEASE Definition: Chronic obstructive pulmonary disease (COPD) is a group of respiratory diseases that characterized by progressive obstruction of airways leading to dilatation & destruction of alveoli. Fig.39 a: COPD pathology & cause  Causes: 1. SMOKING: Prolonged tobacco use causes lung inflammation and destroys alveoli. 2. Air pollutions. Page 76  Fig.39b: Hubly Bubly as important cause for COPD  Symptoms: 1. Progressive shortness of breath (dyspnea). 2. Wheezing. 3. Cough.  Complications: 1. Emphysema: is a long-term, progressive disease of the lung(s) and occurs when the alveolar walls are destroyed along with the capillary blood vessels that run within them. This lessens the total area within the lung where blood and air can come together, limiting the potential for oxygen and carbon dioxide transfer. 2. Respiratory failure. Page 77 3.Interstitial lung Disease: This is group of diseases that causing interstitial lung fibrosis& lung stiffness leading to shortness of breath +/- cyanosis.. 1. Cryptogenic fibrosing alveolitis. 2. Drugs induce pulmonary fibrosis e.g. Amiodarone, Methotrexate. 3. Radiotherapy induces pulmonary damage. 4. Sarcoidosis. 5. Asbestosis. 6. Autoimmune diseases. DISEASES OF THE PLEURA  Pleurisy: Inflammation of the pleura characterized by sharp pain that increase with breathing and coughing., usually occurring as a complication of a chest diseases such as pneumonia, pulmonary embolism.  Pleural Effusion It is excessive accumulation of fluid in the pleural cavity.  Causes: 1. Disturbed osmotic balance e.g. liver cell failure, nephrotic syndrome ,Congestive heart failure. 2. direct causes either from Pleura itself or surrounding Page 78  structures e.g Bronchogenic carcinoma, Bacterial pneumonia, Pulmonary infarction, tuberculosis.  Diagnosis: a. Clinical examination: Dull in percussion, diminished air entry on auscultation. b. Investigations: Plain chest X-ray. Cat scan chest. Pleural tap with pleural fluid analysis. Fig.40: Left pleural fluid collection  Pyothorax (Pleural empyema) : It is accumulation of pus in the pleural cavity due to spreading of infection to the pleural sac.  Diagnosis: same as pleural effusions except that fever &rigors are usually present & pleural tap demonstrates pus. Page 79