Week 3 Lectures: Hypertension PDF

**[Week 3 lectures]** **[Dr Simcock lecture 1]** **Hypertension** - Increased blood pressure - Associated with high level of health care expenditure - Controlling hypertension reduces risk of stroke, kidney disease, heart failure and coronary heart disease **Silent Killer** - Crea...

**[Week 3 lectures]** **[Dr Simcock lecture 1]** **Hypertension** - Increased blood pressure - Associated with high level of health care expenditure - Controlling hypertension reduces risk of stroke, kidney disease, heart failure and coronary heart disease **Silent Killer** - Creates greater afterload, myocardium enlarges, and heart weakens - Accelerated process of **atherosclerosis** - Affects cardiac output and perfusion to tissues **Types of hypertension** - Primary 1. Essential (no underlying cause) 2. Lifestyle factors 3. Physical activity and weight loss is first step for treatment 4. Combination of genetic and environmental factors 5. Hereditary, dietary (cholesterol and saturated fats), obesity, age, diabetes mellitus, stress, smoking - Secondary 1. Underlying causes, for example kidney disease **Obesity** - Mechanical stress- increased vessel length to sustain excess body mass - Atherosclerosis due to poor diet - Physical stress on vasculature, impeding venous return **Ace Inhibitors (type of antihypertensive drug therapy)** - Captopril, enalapril, lisinopril, perindopril and remipril - Blocks angiotensin converting enzyme, antagonizing angiotensin 1 conversion to angiotensin 2 - Reduces constriction of arteries - Reduces sodium and water retention by kidneys, decreases circulating BV **Angiotensin 2 receptor blockers** - Azilsartan, candesartan, eprosatan, irbesartan, iosartan, losartan, Olmesartan - Inhibit the action of angiotensin 11 - Vasodilation of arteries and reduces Na and H2O retention by kidneys, decreases circulating blood volume **Beta blockers** - Reduce the effect of noradrenaline - Block site of action (beta 1 receptors) - Reduce heart rate and cardiac output **Calcium channel blockers** - Disrupt movement of ions through calcium channels responsible for contraction of cardiac muscle - Reduce force of contraction - Vasodilation - Reduce heart rate - Reduce aldosterone production- decrease blood volume **Diuretics** - Reduce water and sodium retention - Decrease blood volume **Atherosclerosis** - Endothelium is injured - Lipids accumulate and oxidise in the tunica intima - Smooth muscle cells proliferate and a fibrous capsule forms - Plaque protrudes into vessel lumen **Stable vs unstable plaque** - Atherosclerotic plaques can have two basic impacts: - Stable plaque 1. Restricts blood flow and oxygen to heart 2. Progressive weakening of heart pumping 3. Angina, silent myocardial ischemia and variant or vasospastic angina - Unstable plaque 1. Rupture 2. Blood clot formation (thrombis) 3. Coronary occlusion 4. Myocardial infarction and unstable angina **Consequences (of plaque)** - Stiffened artery walls 1. Hypertension - damage arterial walls 1. Thrombus (clot formation) 2. Injured epithelial cells make less anti-thrombotic chemicals - Increases risk of myocardial infarction and stroke - Responsible for pain occurring with ischemic heart disease, angina - Risks include, Increasing age, male, family history, dyslipidemia, hypertension, smoking, physical inactivity, diabetes and obesity **Angina Pectoris** - Term used for chest pain - Determined by the degree to which coronary arteries are compromised - Stable, unstable, variant **Anginal pain** - The pain associated with angina is typically described as being constricting, squeezing or suffocating. Associated with myocardial ischemia - Pain **mainly** felt in chest, but may radiate to left shoulder, jaw or arm **Angina** - Stable- result of atherosclerotic plaque constricting blood flow adequate at rest, exertion causing pain - Unstable- result of atherosclerotic plaque and an associated thrombus, greater degree of constriction. Compromised even at rest - Varient- unexplained spasms constricting blood flow. Can occur at any time, not just with exertion **Lifestyle modification** - Stop smoking, stress reduction, regular exercise, limit cholesterol and saturated fats, weight reduction and avoid cold and other physical stresses - Immediate cessation of activity if an attack starts- sit or stand quietly rather than lie down **Glyceryl trinitrate (GTN)** - Potent vasodilator. Decreases preload by increasing venous capacity. Reduces ventricular filling pressure and arterial blood pressure - Helps open collateral vessels in ischaemic areas of the myocardium, improving coronary blood flow **Arteriosclerosis** - Thickening of arterial walls and loss of elasticity of blood vessels - One form of arteriosclerosis is atherosclerosis where lesions, known as atherosclerotic plaques, form in the blood vessel wall - High blood lipid and cholesterol levels are a risk factor, but disease has inflammatory component - Drug therapy can be used to manage lipid levels - Fibrous plaques can block the lumen of the blood vessels, reducing blood flow - The rupture of a plaque will trigger blood clot formation, and potentially stroke **Lipids** - Lipoproteins 1. Package lipids so they can be transported through blood (water-soluble medium) 2. Triglyceride and cholesterol 3. HDL and LDL **Acute and chronic coronary syndromes** STEMI event 1. ST correlates with ventricular contraction and T with ventricular relaxation 2. ST elevation indicated transmural infarction (full thickness of the heart wall) 3. Major risk factors for ST-elevation myocardial infarction are dyslipidemia, diabetes, mellitus, hypertension, smoking and family history of coronary heart disease **Patient management**- Resolve occlusion, Reperfuse the ischaemic myocardium, minimize infarct size and relieve symptoms - Immediate management is: Oxygen therapy, analgesia, aspirin, beta-blocker, nitrates, opioids, if there is ECG evidence of infarction, then thromblytic agents are indicated to achieve reperfusion, angioplasty, stents **Treatment with drugs** - To reduce the risk of thrombosis and a myocardial infarction: 1. Anti-platelet agents (aspirin) 2. Anticoagulants (warfarin) **Heart Disease** Heart failure causes - Hypertension, coronary artery disease, arrhythmias, valvular heart disease, excessive alcohol intake and hyperthyroidism Chronic heart failure - In heart failure there is low cardiac output - Primary left ventricle - Two types of failure calculated from ejection fraction 1. Failure with preserved ejection fraction 2. Failure with reduced ejection fraction - Prognosis is poor, especially in patients showing systolic failure **Normal EF** \ [\$\$ejection\\ fraction = \\frac{\\text{Stroke\\ volume}}{\\text{end\\ diastolic\\ volume}}\$\$]{.math.display}\ - Normal EF is 50-60% **Preserved ejection fraction** - Cardiac output low - EF is normal but stroke volume is abnormally low - Diastolic failure- heart not relaxing and low filling **Reduced ejection fraction** - Lower than 45% and stroke volume is low - Heart is not contracting well=weak muscle HFrEF/Systolic failure - Evidence of congestion, low cardiac output Compensatory mechanisms - Sympathetic activation - Baroreceptors sense low BP - Cardio accelerator increase heart rate and increase contractility to increase CO - Vasometer centre increases and vasoconstriction increases PVR - This increases the workload of the failing heart - Activation of the RAAS - Reduced blood flow to kidneys 1. Increases angiotensin 2 2. Increases aldosterone - Angiotensin 2 directly constricts blood vessels, increasing blood pressure - Aldosterone cause Na+ and water retention, increasing blood volume - Preload increases, which should increase contractility and CO, but has little effect in patients with CHF and workload increases **Principles of treatment for heart failure with reduced ejection fraction** - Reduce hypertension 1. ACE inhibitors 2. Angiotensin receptor blockers - Reduce cardiac workload 1. Beta blockers - Usually treat cause - Drugs for reduced ejection fraction not always useful for preserved EF **Signs and symptoms- left sided failure** - Fluid builds up in lungs - Pulmonary hypertension - Little peripheral oedema **Right sided failure** - Fluid builds up in systemic system - Peripheral oedema - Right sided failure leads to low CO from left side as well Acute rheumatic fever - Acute, generalized inflammatory reaction to group A streptococcal infection - Repeated bouts of ARF due to re-infection with group-A streptococci lead to RHD - Management of RHD leads to: 1. Decreased average number of people living within one home 2. Better hygiene 3. Improved access to penicillin-based antibiotics **Autoimmune response to rhematic fever** - Group A streptococcus (GAS) penetrate epithelium - B- cells and T-cells responses to GAS affect host - Causes fever, arthritis - Affected sites include myocardium and endocardium **Inflammatory damage to valves (RHD)** - Repeated infections lead to more progressive damage - Myocardium recovers function - Valve thickened and calcified - Don't close properly- regurgitation - Lowers stroke volume - Reduces cardiac output **Vegetations** - Vegetations form on valves=scarring-stenosis - Valves become rigid - Don't properly open - Poor filling of ventricles **Complications** - Nodules in valves- infective endocarditis - Increase the workload of the heart- heart failure (usually HFrEF) - Overstretched atria- atrial fibrillation - Fibrillation-clots-ischaemic stroke **ARF and RHD management strategies** - Four levels of prevention: primordial, primary, secondary and tertiary 1. Primordial= stops GAS infections (environmental) 2. Primary= stop infection becoming ARF (antibiotics) 3. Secondary prevention- prevent repeat ARF infections, injection of benzathine penicillin into a large muscle every 4 weeks, for 10 years or until patient turns 18 4. Tertiary prevention treat pathology of RHD (valve replacement, management of heart failure) **[Dr Liddell Lecture 1]** **Metals** - Electron sea model- delocalized "sea" of mobile valence electrons around a regular but non-rigid array of metal ions (nuclei +core electrons) - Metal properties- solids (liquids), malleable, ductile, conductors, moderate melting point, high boiling point and crystallize in one of three structures **Crystal structures** - May be represented by 3D lattices where each lattice point represents a repeating location for a motif of atoms. We need to place one atom at lattice point - Unit cell is the smallest, regularly repeating parallelepiped from which a crystal lattice is formed by parallel displacements in three dimensions **Metal Structures** **Metal Strength** - Single crystal- 1 grain, outer surface of microcrystal has flat faces - Polycrystalline- metal made of crystals of different size, orientation, shape. Under stress the dislocations propagate to edge but hard to move across grain boundary - Smaller grains indicate higher strength - Dental metals- alloying, cold working, precipitation hardening, age hardening etc to increase strength **Metal alloys** - Alloy- material with metallic properties resulting from the melting together of two or more elements, 1 element is metal. i. Alloys are prepared at the final stage in metallurgy where the required alloying elements are added to the molten metal - Brass- 67% Cu, 33% Zn alloy 1. Solution alloys- homogenous mixtures components dispersed randomly, uniformly a. Substitutional alloy- atoms of the minor component substitute for atoms in the bulk structure. Atoms of similar size and chemical bonding tendencies b. Interstitial alloy- one atom type is much smaller and fits into the interstices of the bulk structure - Properties change such as- luster, malleability, ductility, hardness, corrosion, melting point **Noble (inert) dental alloys** - Many dental alloys are classified by noble metal content - Base metals- non-noble are more easily oxidized - Classifications- HN (40%), N (\>25%), PB (\ - The standard potentials for the half-reactions cannot be measured independently and so it is necessary to have a standard to which they are relative - The sign of Ecell tells us whether the reaction is spontaneous or not - Positive Ecell means spontaneous - This comes about from the relationship between Ecell and the Gibbs free energy **Voltaic cell** - The flow of electrons can be used as a source of energy **Concentration cells** - Ecell depends on concentrations in either half-cell, hence the name concentration cell - A voltage exists as there is a charge difference between the two half cells - A proton gradient is a concentration cell **Corrosion of iron** - Rusting of iron progresses by a series of redox reactions that includes the oxidation of Fe to Fe2+ and the reduction of O2 to O2- - Followed by the subsequent oxidation of Fe2+ to Fe30\\+ as Fe2O3 - In rusting, the Fe acts as anode and Fe also acts elsewhere as a cathode where O2 is reduced - Rusting is accelerated in electrolyte solutions as ions enhance the electrical circuit allowing passage of a current **Rusting of Fe --** Fe is both anode and cathode in the process, but Fe is lost only at anode **Corrosion in the oral cavity** - Saliva acts as an electrolyte and allows effective galvanic cells to be set up. Conditions that can contribute to corrosion: moisture, electrolytes, changing pH - Electrode potentials are altered in dental devices made of metal because of: 1. Differences in metals 2. Inhomogeneities in metallic structures 3. Differences in electrolyte composition 4. Differences in oxygen concentration **Activity series** - A listing of redox half-reactions in order of decreasing ease of oxidation. At the top of the list, oxidation occurs readily, active reducers. At the bottom reduction happens **Dissimilar metal corrosion** - In the oral cavity, a galvanic cell can be established due to differences in electrode potential between 2 metals in close proximity and saliva electrolyte - Difference in electrode potentials causes a current-largest when the dissimilar metals are in contact 1. Cause: dissimilar metals have different activity or redox potential **Dental Pain** - The short circuit between foil in contact with fillings creates a current which is sensed by the nerve of the tooth **Concentration cell corrosion** - The concentration of oxygen varies depending on location-open versus deep in biofilm. This creates anodic and cathodic regions on metallic devices - This is enhanced when the electrolyte concentration varies based on location- food debris location versus saliva **Crevice corrosion-** the crevice when a metal implant meets bone provides a low oxygen environment and this allows active ion loss to occur in the crevice **Stress corrosion-** originates at locally stressed sites (e.g. pits)- anodic - Cold working an alloy- stressed sites (corrosive environment: Sulfides, acid) - Corrosion follows this process: pits=\ crack initiation=\>crack propagation - Requires a corrosive environment in combo with local stresses - Electrochemical cells can be set up between deformed regions (anode) and unaltered regions (cathode) with saliva as electrolyte - Occlusion is the contact relationship between maxillary and mandibular teeth when the teeth are in function/parafunction - Static occlusal relationship 1. Relationship between maxillary and mandibular teeth when jaws are closed - Dynamic occlusal relationship 1. Relationship during various jaw movements **What makes an occlusion** - occlusal contact between maxillary and mandibular dentition are affected by skeletal base relationship, development of the maxilla and mandible and direct factors affecting the development, position and shape of the teeth themselves **Neuromuscular aspect/anatomy of occlusion** - Principle and accessory muscles of mastication/jaw movements - TMJ - Skeletal relationship - Teeth **Neuromuscular aspect/anatomy of occlusion** **TMJ** A diagram of the anatomy of the human body Description automatically generated **Centric relation-** a maxillomandibular relationship, independent of tooth contact, in which the condyles articulate in the anterior-superior position against the posterior slopes of the articular eminences **Centric occlusion**- the occlusion of opposing teeth when the mandible is in centric relation; this may or may not coincide with the maximal intercuspal position **Retruded position**- position of condyle in posterior most position during TMJ movement **Retruded contact position**- initial contact of a tooth or teeth during closure around a transverse horizontal axis **Intercuspal position**- cusp to fossa relation of maxillary and mandibular teeth **Development of occlusion (primary-permanent dentition)**  **Overjet and overbite** - Standard maxillary arch outline is relatively wider than mandibular arch - Maxillary teeth overhangs mandibular teeth in a standard centric occlusion - The permits overjet (horizontal overlap of maxillary teeth over mandibular teeth) or overbite (vertical overlap of maxillary teeth over mandibular teeth) **Molar relationship** - **Class 1 (orthognathic)-** considered normal occlusion. Maxillary 1^st^ molar MB cusps lies over mid buccal groove of mandibular first molar - **Class 11 (retrognathic)-** Maxillary teeth are relatively forward in relation to mandibular teeth in comparison to class 1 - **Class 11, division 1-** protruded anterior teeth - **Class 11, division 11-** one or more retruded maxillary anterior teeth - **Class 111 (prognathic)-** lower molars are forward comparative to class 1 and do not fit their corresponding upper molars - Class 11 and 111 are considered malocclusion **Curves/planes of occlusion** **Curve of Spee** - **Cure of Spee-** refers to the anteroposterior curvature of the occlusal surfaces-following the tip of cuspids, bicuspids and molars. **Curve of Wilson** - The occlusion should be spherical in frontal plane as well - Refers to the occlusal curve on both sides of the arch following the cusp tips of mandibular teeth (concave). In maxillary teeth it represents as convexity - The plane enables smooth functioning of lateral excursions without interference **Dynamic occlusion-on rotation** - Hinge- opening and closing - Mouth opening on an imaginary horizontal hinge axis through head of the condyles **Dynamic Occlusion- translation** **Lateral occlusion- (side to side excursions and lateral closing)** **Working side/non-working side** - During lateral excursions, the side of the mouth to which the mandible has moved is known as the working side, while the side of the mouth from which the mandible has moved away is known as the non-working side - When the condyles are most posterior and superior position in the glenoid fossa, the mandible is said to be in the terminal hinge axis position **Functional cusps- (working cusps)** - Cusps that occlude with the opposing teeth in centric occlusion - In normal occlusion, the palatal cusps of the maxillary posterior teeth and the buccal cusps of the lower posterior teeth **Non-**functional **cusps** - Do not occlude with the opposing teeth in centric occlusion - In normal occlusion, the buccal cusps of the upper posterior teeth and the lingual cusps of the lower posterior teeth **Occlusion in restorative treatments** - Two approaches by which to manage a patient's dentition to restore - Proper function long-term and the analysis of occlusion is critical to ensure success: 1. Conformative approach- no change to pre-existing occlusal relationships in the three planes: antero-posterior, vertical and horizontal 2. Re-organised approach- changing pre-existing occlusal relationships to rehabilitate major discrepancies ("complex" treatment) **Assessing occlusion** - Patient's occlusal relationships both static and dynamic need to be analyzed prior to commencing any restorative procedure in the conformative approach of providing dental care - Verify that no changes have been made at the completion of the restorations - Checking direct occlusal contact relationships in the patient's mouth can be done in various ways 1. Articulating paper 2. Shimstock 3. Clinical observation **Instrumentation to assess occlusion** **Articulating paper** - Available in various thicknesses ranging 40-200 nanometers in different colours and shapes (generally long rectangular for quadrant, or broad square/arch shaped for bilateral applications) - Thinner articulating papers are more accurate but can be difficult to manipulate and fold **Articulating Foil**- Thinnest foils for fine occlusal adjustments of coronal restorations and more accurate analysis - Shimstock (8 nanometers thick) - Trollfoil (4.58 nanometers thick) **What makes an ideal articulating paper or foil** - Precise marking, no smudging- to ensure accurate adjustments are made - Tear resistant-able to withstand gentle tugging whilst stuck between teeth - Water resistant- doesn't go to mush after the first use - Static-free- doesn't stick onto itself (especially the thinner ones) - Marks pressure dependent- the heavier the contact, the darker the colour - Marks highly polished surfaces such as gold, porcelain, ceramics whilst wet **Holders** - To hold articulating paper for the ease of use of articulating paper **Visual assessment** - Visually assess dental contacts around the arch before removing the old/damaged restoration and take a mental note - After restorations, its important to establish occlusion as required **Clinical procedure** - Check the occlusion before starting and after finishing the restoration - Static assessment i. Have the patient tap their teeth together and keep closed (one colour) - Dynamic assessment i. Have the patient close and slide side-side and back to front (in different colours) - When checking the new restoration, use words such as gently close down and light tap, not bite - The patient will most likely be numb on the side of restored and will not be able to gauge how fast or strong they close together - The goal is to have the original occlusion restored (conformative) 1. To achieve balance once again 2. The timing of the teeth meeting together - Note that the goal is not to remove all the marks but rather, reduce the heavy areas until balance and coincidental timing is achieved