Clinical Pathological Aspects of Cardiovascular Disease 2023 PDF

Why? 7 million people in the UK living with cardiovascular disease Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure Hypertension Depending on criteria said to be present in 20-30%...

Why? 7 million people in the UK living with cardiovascular disease Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure Hypertension Depending on criteria said to be present in 20-30% of the adult population Persistently raised blood pressure > 140/90 mm Hg 90% No cause found = Primary / Essential hypertension 10% Cause found = Secondary hypertension Primary (Essential) Hypertension Most common cause of preventable disease in developed world Normally detected between 20-50 years of age Primary (Essential) Hypertension Multifactorial Aetiology Genetic factors Environmental Obesity (ensure correct cuff size) Alcohol Salt intake Stress Humoral mechanisms Insulin resistance – link between diabetes and hypertension Secondary Hypertension Renal disease E.g. diabetic nephropathy, chronic glomerulonephritis, adult polycystic disease Autosomal dominant polycystic kidney disease is a disorder Pregnancy in which there is an enlargement of the kidneys with multiple cyst formation. Endocrine disease E.g. Conn’s syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing’s syndrome, acromegaly Drugs E.g. Cortocosteroids, oral contraceptive pill Coarctation of the aorta Diagnosis of Hypertension Measurement of blood pressure on at least 3 occasions over 3 month period Patients often require a 24 hour monitor Treatment Secondary hypertension – treat cause if possible Primary / Essential hypertension General advice (BHS) Weight loss Increase exercise Reduce alcohol Stop smoking Reduce salt intake Increase fruit and vegetable intake Treatment 2 Medical treatment ACE Inhibitors (eg captopril) Angiotensin II receptor blockers (eg candesartan) B β-blockers (eg atenolol) Ca channel blockers (eg nifedipine) Diuretics (eg bendroflumethiazide) Hypertension - complications Heart failure Stroke – cerebrovascular accident (CVA) Coronary artery disease / Myocardial infarction (MI) Renal failure Peripheral vascular disease Hypertension- dental relevance Minimise stress and pain to minimise further increase in BP which may precipitate CVA, MI No problem with adrenaline in LA (as long as intravascular injection avoided) Controlled hypertensive – treat as normotensive Uncontrolled hypertensive (>140/90mmHg) – delay elective treatment. Refer to GP. Severe hypertension (>180/110mmHg) – Refer urgently to GP or hospital Post-operative bleeding more likely Patient likely to be taking aspirin Hypertension – dental relevance 2 Oral manifestations ACE inhibitors Loss of taste Angioedema Lichenoid reactions β-blockers Lichenoid reactions Ca channel blockers Gingival overgrowth Diuretics Xerostomia Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure What is a “good ratio?” Intimal layer Scavenger receptors LDL into intima Oxidised, sends chemotactic messages to monocytes Ingestion of LDL by monocytes / macrophages Death of lipid containing macrophages, spillage of lipid and cholesterol Stimulation of smooth muscle cell migration and connective tissue synthesis OEL IEL Blue = collagen, red = smooth muscle, black = elastin https://www.youtube.com/watch?v=Na6-kP9VYCU Thrombosis happens when a blood clot, or thrombus, grows in blood vessels. This can reduce blood flow. An embolus is any foreign material that travels within the body. If it becomes stuck and severely blocks the flow of blood, the issue is called an embolism. Ischaemia Infarction Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure Clinical aspects of IHD Inadequate O2 supply to meet demands of the heart Most common cause of death in Western world accounting for 35% of total mortality. Aetiology – atheromatous plaque within coronary arteries causing constriction to blood flow Risk of plaque rupturing leading to acute thrombus and MI IHD – Risk Factors Unmodifiable Age Male gender Family history Modifiable Hyperlipidaemia Smoking Hypertension Diabetes Obesity Lack of exercise High alcohol intake Stress OCP Angina ANGINA PECTORIS- reduced O2 perfusion of the cardiac muscle resulting in: Strangling feeling in the chest. (Greek ‘Angina’= Strangling, Latin ‘Pecta’ = chest) Breathlessness Pain radiating to the jaw and the left arm Pain resolves in minutes following rest and GTN Angina – dental relevance Polypharmacy Side affects of these medications - how will they affect the patient and what you plan to do to them Aspirin - bleeding tendency Beta Blockers/Ca channel blockers - mucosal disease Nicorandil - oral ulceration Myocardial Infaction Symptoms: Central strangling pain lasting longer than 15 minutes Pain radiates to the neck, jaw and left arm Nausea, vomiting Signs: Grey tinge Sweating Tachycardia Myocardial Infarction Management Sit patient up Calm and relaxed approach Dial for an ambulance/crash team Administer O2 and GTN (repeat every 10 minutes) Aspirin 300mg PO crushed or chewed Entonox if available Monitor pulse and oxygen saturation MI- Dental Relevance Dental treatment may precipitate angina / MI - need to minimise stress and pain May present as jaw pain May use GTN prophylactically Unstable angina – delay elective treatment until controlled Likely to be taking aspirin Oral manifestations of drugs - Ca channel blockers - gingival overgrowth - β-blockers – lichenoid reactions - Nicorandil – oral ulceration Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure Clotting Thrombosis Haemostasis occurring in the wrong place and at the wrong time Changes in the surface of the vessel Changes in the blood flow Atrial fibrillation happens when abnormal electrical impulses suddenly start firing in the atria. Changes in the constituents of the blood Increase procoagulant factors Procoagulant factors from malignant tumours Increased platelet count and adhesiveness/ aggregatibility Decrease in anticoagulant factors Increased viscosity of the blood Hypertension Pathology of atherosclerosis Clinical aspects of ischaemic heart disease (angina, MI) Pathology of thrombosis and embolism Clinical aspects of heart failure Clinical aspects of heart failure Heart failure is when the heart is not able to pump blood at a rate that the bodies requirements The heart can not fill quickly enough to match demand or where it can not pump the blood out Types: left sided, right sided or both Why? Pump failure eg. heart muscle disease, restricted filling, inadequate heart rate Excessive preload eg. Mitral regurgitation, fluid overload Chronic excessive afterload eg aortic stenosis, hypertension Clinical aspects of heart failure Heart failure is when the heart is not able to pump blood at a rate that the bodies requirements The heart can not fill quickly enough to match demand or where it can not pump the blood out Types: left sided, right sided or both Why? Pump failure eg. heart muscle disease, restricted filling, inadequate heart rate Excessive preload eg. Mitral regurgitation, fluid overload Chronic excessive afterload eg aortic stenosis, hypertension