Hypertension Lecture Notes PDF

HYPERTENSION Dr. Raymond R. Maeda OPTM 5175 Learning Objectives Students will be able to... – Become familiar with epidemiology of HTN – Understand systolic/diastolic pressure (BP readings) – Become familiar with staging of HTN – Understand the risk factors and pa...

HYPERTENSION Dr. Raymond R. Maeda OPTM 5175 Learning Objectives Students will be able to... – Become familiar with epidemiology of HTN – Understand systolic/diastolic pressure (BP readings) – Become familiar with staging of HTN – Understand the risk factors and pathophysiology of Essential HTN – Understand the impact of the Sympathetic Nervous system and Renin-Angiotensin- Aldosterone System affect blood pressure – Understand the role of the Kidney related to hypertension – Understand the different causes of Secondary HTN – Recognize signs and symptoms of hypotension – Understand how Arteriosclerosis and Atherosclerosis are related to HTN – Become familiar with significant ocular complications related to HTN – Recognize the different stages of Hypertensive retinopathy – Be familiar with the different treatment modalities  Approximately 1.28 billion adults (30-79yo) worldwide have HTN In the US 1 in 3 adults has HTN – 2/3 living in low- and middle-income countries 46% of adults with HTN are unaware that they Hypertension have the condition. ~ 1 in 5 adults have it under control (HTN) More prevalent in men than women (not dramatically different) More prevalent in non-Hispanic blacks (57.2%) than non-Hispanic White (42.6%) or Hispanic (43.7%) adults. Based upon the American College of Cardiology/American Heart Association (ACC/AHA) hypertension is defined as a blood pressure > 130/> 80 mmhg.  HTN is an attributable risk factor in 41% of all CVD deaths from MI, heart failure, and stroke. An increase in BP of 20mmhg (systolic) or Hypertension 10mmhg (diastolic) is associated with a (HTN) doubling of the risk of CVD death regardless of age. In middle-age patients with HTN there is a known increase in the development of chronic kidney disease and dementia in later life. Who gets Hypertension? By age... – 18 to 39yo 22.4% of adults in this age group – 40 to 59yo 54.5% of adults in this age group – > 60yo 74.5% of adults in this age group By gender... – More common in men than women in younger age groups but becomes less pronounced with age Other factors... – Ethnicity: Non-Hispanic African- Americans are more likely to have HTN than Caucasians, Asians or Hispanic people HTN What is blood pressure? – Is the pressure of blood pushing against the walls of your arteries as it carries blood – What do the numbers mean? Systolic / Diastolic Systolic – is the pressure in your arteries when the heart beats (contracting) Diastolic - is the pressure in your arteries when the heart is at rest (between beats/refilling) “Normal” = 120/80mm Hg Guidelines on screening for HTN have been issued by many organizations – Joint National Committee (JNC) and American of Cardiology / American Heart Association (ACC/AHA) Others include: European Society of Hypertension (ESH) / European Society of Cardiology (ESC), Depart of Veterans Affairs (VA) / Department of Defense (DoD) ACC/ AHA Guidelines Atherosclerotic Cardiovascular Disease Risk Estimator (*developed by ACC and AHA) It is a tool to calculate a patient’s 10-year risk for developing atherosclerotic cardiovascular disease (ASCVD), which includes events like heart attack or stroke based on factors: age, gender, ethnicity, cholesterol levels, blood pressure and smoking status. The calculator helps guide treatment decisions, including whether to start a statin based on a patient’s calculated risk level. **10-year risk for ASCVD is categorized as: Low-risk ( 180 and/or the diastolic blood pressure is > 120. 2 Subcategories: – Hypertensive Emergency Immediate Referral – Hypertensive Urgency Consult with PCP Hypertension (HTN) Mild/moderate HTN rarely causes symptoms. As blood pressure continue to elevate and go untreated patients can experience vague symptoms: – HA, blurry vision or dizziness Severely elevated BP can cause more severe symptoms due to acute, severe, and life-threatening complications: – Papilledema, stroke, encephalopathy, acute kidney injury and heart failure It is important to use proper technique when assessing blood pressure Assessing blood pressure Errors in blood pressure management Inappropriate cuff size – Too small of a cuff can increase readings by 5 to 10mmhg – Too large of a cuff can decrease readings by 5 to 10mmhg Poor cuff placement – Cuff that is too loose/not placed properly: false high readings – Deflation of the cuff too slow = false high or too fast = false low Recommendations based upon blood pressure... (*based on ACC/AHA classification) Stage I (130-139 / 80-89) – Recheck BP in 5 minutes – Assess patient’s overall health status (any h/o MI, angina, stroke, renal disease or other systemic concern) – Document / Provide pt education – Pt should be advised to recheck at home and contact PCP if necessary. Stage II (> 140 / > 90) – Same as above – Consider consulting with pt’s PCP office. Beware of White Coat Hypertension Also known as “white coat syndrome,” is a condition where a patient’s blood pressure spikes in medical settings due to anxiety. It’s not uncommon, and while it might seem harmless, it can indicate that their blood pressure might also rise in other stressful situations. Patients who experience white coat syndrome should monitor their blood pressure at home and keep a record of their readings. This data will help their doctor determine if they need treatment outside of the clinical environment.  HTN Primary Hypertension is most likely due to multiple factors: (95%) – It is multi-factorial and does not have one distinct cause: age, diet, excess caffeine/sodium intake, FmHx, obesity, alcoholism, sedentary lifestyle – Not due to a medical condition. Secondary Hypertension is when there is an identified cause: – Kidney disease, Endocrine disorders, certain medications or changes to blood vessels (aorta / kidney arteries) Governing factors in determining blood pressure include mean arterial pressure (MAP), cardiac output and peripheral resistance. – Cardiac output (CO) is the product of the heart rate times stroke volume ejected with each beat, and MAP is the product of CO and total peripheral (vascular) resistance The goal of the cardiovascular system is to maintain a constant flow of blood to the vital organs. Homeostasis HTN PERIPHERAL RESISTANCE Increase in blood pressure may result from changes in arterial tone due to increased alpha- adrenergic stimulation and changes in vessel wall elasticity reduced by vascular smooth muscle contraction. Atherosclerosis and Arteriosclerosis can also contribute to increased peripheral resistance. Sympathetic stimulation can occur with physiologic stressors such as exercise, psychological stress, and pharmacological triggers (stimulants). The transient rise in blood pressure during the day due to exercise is beneficial to maintain arterial elasticity. Chronic sympathetic stimulation may be harmful – individuals living in fear, under high stress, illicit drugs can cause a sudden increase in blood pressure and muscle tone. Primary/Essential HTN In younger patient Cardiac Output (Heart Rate x Stroke Volume) is typically elevated in older patients there is increased Total Peripheral Resistance (Systemic Vascular Resistance) and increased stiffness of the vasculature play a dominant role (arteriosclerosis). Primary and Secondary HTN can co-exist – if there is an acute worsening of BP, a new secondary cause should be considered. Primary/Essential HTN Develops gradually over time – pt can be asymptomatic Risk factors – Age (especially after 45 in men and 65 in women) – Smoking: chemicals can affect the walls of the arteries – Alcohol intake (in excess): damage the heart (not able to pump as efficiently) – Obesity: increased weight means more blood is needed to supply one’s body with oxygen and nutrients. – Lack of physical activity contributes to obesity. – Poor diet (esp high in sodium/salt): more salt = retain more fluid = increased BP. – Genetics: not a modifiable risk factor. Primary/Essential Hypertension Age – See increased arterial stiffening/hardening due to loss of elastin fibers in large arteries and a buildup of stiffer collagen fibers – Isolated systolic hypertension (80% are over 65yo) Where only the systolic blood pressure becomes elevated Theory is that it is due to vessel wall changes that increase the load on the left ventricle and impacts coronary blood flow, which leads to left ventricular hypertrophy, coronary ischemia and heart failure. Smoking – Nicotine constricts the blood vessels leading to elevated BP. – Carbon monoxide in tobacco products damages the lining of the blood vessels, making them less elastic. – Oxidative stress damages the blood vessels and leads to inflammation. Primary/Essential Hypertension Alcohol Intake – Causes vasoconstriction which causes the heart to work harder to pump blood Having more than 2-3 drinks in one sitting raises one’s blood pressure for a short time. Obesity – Typically assessed by calculating the BMI (body mass index (>30) – Individuals are 2-3x’s more likely to develop HTN – Different mechanisms Increased sympathetic nervous system activity (increase in release of epinephrine and norepinephrine) *also activates the RAAS – Due to chemicals released from adipose tissue (leptin) Increase in insulin resistance – Occurs due to different reasons: increased SNS activity, RAAS activation and impaired vascular function. Increased sodium retention – caused by activation of the RAAS Changes in blood vasculature Renal compression: kidneys need a higher-than-average blood flow to function properly, which leads to elevated blood pressure. Primary/Essential Hypertension Sedentary Lifestyle – Lack of physical activity / prolonged sitting are correlated with elevated blood pressure. Your metabolism slows down impacting blood flow Typically coincides with other risk factors: obesity, unhealthy diet, and excess alcohol consumption Poor Diet – Especially one that is high in sodium and low in potassium is a risk factor. High sodium intake – found in processed foods – Kidneys have to work harder to remove sodium from the bloodstream. This leads to water retention, which leads to increased blood volume returning to the heart. – Increases the “pre-load” and the stroke volume which lead to increased Cardiac Output (CO) – Increase potassium intake (fruits/vegetables) to improve blood pressure High in saturated fats – contributes to HTN risk (cholesterol) High in sugar – contributes to weight gain (added sugar = high calorie with no nutritional value) Primary/Essential Hypertension Genetics – Patients with 2 parents with HTN have a 2.4x increased risk in developing HTN. – Tend to see it as factor in younger patients who develop HTN. – The genetic inheritance pattern is not well known at this time but we do see genetics in women more than men when it comes to HTN. Sympathetic Nervous System (SNS) Manages our “fight-or-flight response” Regulates blood pressure by influencing the vasculature, kidneys and heart. SNS is activated by the hypothalamus by sending signals to the adrenal glands which release epinephrine into the bloodstream – Causes increased heart rate, contractility, vasoconstriction and blood pressure Affecting the beta-1-adrenergic receptors located in the SA node and cardiac muscles. Less affect on the alpha-adrenergic receptors in the heart (coronary blood vessel constriction) Renin-Angiotensin-Aldosterone System (RAAS) A hormonal system in the body (kidneys) that primarily regulates blood pressure by controlling fluid and electrolyte balance through the action of different hormones: – Renin, Angiotensin II and Aldosterone When blood pressure drops, the kidneys release renin, which leads to a cascade of reactions that will ultimately lead to vasoconstriction and increased sodium absorption - - leading to the elevation of blood pressure. Main function of RAAS = maintain BP by regulating blood volume and vascular tone. Renin-Angiotensin-Aldosterone System (RAAS) Hormones being released: – Renin: enzyme secreted by the kidneys when blood pressure drops – Angiotensinogen: a protein produced by the liver that is converted to Angiotensin I by renin. – Angiotensin Converting Enzyme (ACE): an enzyme that converts Angiotensin I to the active hormone, Angiotensin II. – Angiotensin II: causes the blood vessels to constrict and stimulates the adrenal glands to release aldosterone. Also causes release of Anti-diuretic hormone from the pituitary gland Causes the kidneys to retain water from the urine, which increases blood volume and blood pressure. – Aldosterone: causes kidneys to retain sodium and water, increasing blood pressure. Renin-Angiotensin- Aldosterone System (RAAS) Why is this important? – Drugs that inhibit the RAAS (ACE inhibitors and Angiotensin receptor blockers) are commonly used to treat high blood pressure by blocking the conversion of Angiotensin I to Angiotensin II or by blocking the Angiotensin II receptor. Basic summary - RAAS 1. When your blood pressure falls, your kidneys release the enzyme renin into your bloodstream. 2. Renin converts angiotensinogen, a protein your liver makes & releases, into hormone angiotensin I. 3. Angiotensin I flows through your bloodstream and gets converted by angiotensin- converting enzyme (ACE) in your lungs and kidneys into angiotensin II, an active hormone. 4. Angiotensin II causes the muscular walls of small arteries (arterioles) to constrict/narrow, which increases blood pressure. Angiotensin II also triggers your adrenal glands to release aldosterone and your pituitary gland to release antidiuretic hormone (ADH, or vasopressin). 5. Together, aldosterone and ADH cause your kidneys to retain sodium. Aldosterone also causes your kidneys to release (excrete) potassium through your urine. 6. The increase in sodium in your bloodstream causes water retention. This increases blood volume and blood pressure, thus completing the renin-angiotensin-aldosterone system. Kidneys / Juxtaglomerular Apparatus Located in the kidneys at the junction of the afferent arteriole and the distal convoluted tubule. In the nephron, the functional unit of the kidney. Each kidney has ~1 million nephrons, which are filtering units of the kidney responsible for producing urine. The Juxtaglomerular Apparatus Juxtaglomerular Apparatus Juxtaglomerular (JG) cells Are smooth muscle cells mainly in the walls of the afferent arterioles. – Contain Renin – Function as mechanoreceptors to sense blood pressure When blood pressure is reduced, the JG cells release renin (*activating the RAAS) Juxtaglomerular Apparatus The Macula Densa cells – Specialized cells of the DCT at the point of contact with the afferent arterioles – Function as chemoreceptors that sense changes to solute concentration and flow rate (filtration) If there is reduced osmolality or low flow rate, there is vasodilation of the afferent arteriole and stimulation of the JG cells to release renin. Increasing the glomerular filtration rate. Conversely, if there is increased osmolality or increased flow rate, there is vasoconstriction of the afferent arteriole. Decreasing the glomerular filtration rate. Glomerulus Small ball-shaped network of capillaries that serves as the primary site of filtration in the urinary system. Filters the blood to remove waste products, excess fluid, and solutes. – Collected by Bowman’s capsule – a thin membrane surrounding the glomerulus. Blood enters thru the afferent arteriole and leaves thru the efferent arteriole. These substances are then excreted as urine. Small molecules pass thru (water, electrolytes, and urea) while retaining larger molecules (RBC’s and proteins) Glomerulus 120ml of blood is filtered / minute or 180 Liters/day We pee 1.8 liters/day Where does the rest of it go? – Absorbed thru the peritubular capillaries (filtrate) – Maintain the appropriate balance of ions, amino acids, glucose, urea Damage to the glomerulus can lead to conditions such as glomerulonephritis, which can cause proteinuria, hematuria and kidney failure. Renal tubules Is a continuous and long pipe-like structure containing the fluid filtered through the glomerulus. The filtrate passing thru the renal tubule ultimately ends at the collecting duct. Components of the renal tubules: – Proximal convoluted tubules lies in the cortex (outer) and is lined by simple cuboidal epithelium with microvilli (brush borders) – Loop of Henle: lies in the medulla (inner) Descending loop Ascending loop – Distal convoluted tubules: lies in the cortex – Collecting duct Blood from the efferent arterioles moves into the peritubular capillaries (surrounds the tubules) – Form an efferent venule which combines with other efferent venules to form the renal vein. Renal Tubules Lt purple– reabsorption Lt orange - secreted Renal Tubule Contains fluid that is filtered thru the glomerulus. It will ultimately end up at the collecting duct. Proximal convoluted tubule – made up of simple cuboidal epithelium / have a large surface area for absorption. – 65% of substances get reabsorbed (back into the capillaries) Loop of Henle (15% of substances get reabsorbed) – Descending & Ascending Loop thinner than the ascending loop. Renal Tubules Distal Convoluted tubule (15% of substances get reabsorbed) – DCT is a target site for diuretic drugs, which inhibit its ability to reabsorb Na+/CL- Collecting tubule/duct (5% of substances get reabsorbed here) We filter most things into the tubules and reabsorb nearly 100% back into the body BUT we secrete specific products back into the tubules. We end up excreting only about 1% of everything we filter.  Secondary HTN (not very common – 5%) – Typically, a younger pt with some underlying disease – Common causes include: R Renal Disease Secondary E Endocrine Hypertension N Neurological disease A Aortic Disease L Little People / Pregnancy S Substances Secondary HTN – Renal Disease Renal artery stenosis (RAS) – Narrowing or blockage of an artery to the kidneys, which can lead to kidney failure or HTN. – Risk factors: Smoking, high cholesterol, high triglycerides, DM, obesity and family hx of heart disease. – HTN is a cause and result of RAS. – Symptoms: early onset of HTN, resistant to tx, & increased urea excretion Renal artery thrombosis – Formation of a clot in a renal artery, which can lead to kidney failure. – Risk factors: Atrial fibrillation, plaque formation, blood clotting disorders and trauma/surgery. – Symptoms: sudden onset flank pain (between rib cage/above the waist), fever, hematuria nausea/vomiting, kidney failure and HTN Secondary HTN – Renal Disease Retinal vein thrombosis – Formation of a clot in a vein to the kidney – Risk factors: trauma/surgery, prolonged bed rest, & certain medications (BCP, HRT.. ) – Symptoms: pain in flank area, swelling/tenderness near kidneys, fever, nausea/vomiting, proteinuria and reduced urine output. Renal artery aneurysm – Bulging/weakened area of a vessel wall. These are small (2cm) and typically asymptomatic. Not common and found during routine diagnostic procedures. – Larger aneurysms (> 2cm) can cause kidney ischemia and HTN. Secondary HTN - Endocrine 2 main organs – Thyroid Can be caused by both overactive and underactive thyroid gland. – Elevated T3 & T4 causes Cardiac output to increase, which typically increases the systolic blood pressure = Systolic Hypertension. – Low T3 & T4 affect the vascular tone = causing vasoconstriction which increased Total peripheral resistance. Typically see elevated diastolic blood pressure = Diastolic Hypertension – Adrenal gland Causes HTN by producing excess aldosterone, which causes the body to retain sodium and water. Conn’s Syndrome Pheochromocytoma – rare tumor in the adrenal glands that causes excess production of epinephrine and norepinephrine. Cushing’s Syndrome – caused by overproduction of cortisol from the adrenal glands, which can cause increased sympathetic activity. Secondary HTN – Neurological Disease Cushing’s Triad – Bradycardia / HTN / Irregular breathing – Is a clinical sign that indicates increased intracranial pressure (ICP) – Occurs when the brain in compressed or herniated, leading to reduced blood flow to the brain. This causes the brainstem to release hormones that increase the heart rate, blood pressure and alter breathing. – Causes: brain tumor, stroke, traumatic brain injury, subarachnoid hemorrhage, and intracranial infection. – This is a MEDICAL EMERGENCY that requires immediate treatment. If left untreated, it can lead to permanent brain damage or death. Secondary HTN – Aortic Disease Coarctation of the aorta – Mainly see in young patients. – Caused by a congenital defect that causes narrowing of the aortic lumen after the left subclavian artery, which leads to elevated blood pressure in the upper extremities. – Symptoms: chest pain dizziness and shortness of breath More commonly see development of aortic aneurysms due to constant elevated BP on the aorta’s wall. Secondary HTN – Little people (pregnancy induced HTN) Pre-eclampsia vs Eclampsia – Mother experiences seizures (Eclampsia) A complication of pregnancy characterized by HTN and protein in the urine (proteinuria) Typically develops 20 weeks of gestation. Cause – not exactly known but can be due to abnormal clotting/vessel concerns, poor placental development/blood flow, generalized inflammation, hormonal imbalances or overall health of the mother (infections DM, metabolic disorders, obesity) Symptoms: severe HA’s, changes in vision, shortness of breath (fluid in lungs), pain in upper abdomen and nausea/vomiting. If left untreated, it can lead to serious/fatal complications for the mother/baby.  Secondary HTN - Substances Pharmacological factors – Some common pharmacologic agents that can impact blood pressure Stimulants – OTC = decongestants (i.e. pseudoephedrine) – Prescription medications used for narcolepsy and ADHD (chemically related to amphetamine) = dextroamphetamine, methamphetamine, and methylphenidate, Non-selective NSAID’s and Cyclooxygenase-2 inhibitors – causes reduction in prostaglandin formation which leads to increases in sodium and water retention. Corticosteroids can cause sodium retention. Overstimulates of mineralocorticoid receptor, resulting in sodium retention in the kidneys. Oral contraceptives may increase blood pressure in some women. Thought to stimulate production angiotensinogen. Serotonin-Norepinephrine Reuptake Inhibitors are used in tx of depression and anxiety disorders. They are thought to increase levels of norepinephrine. Immunosuppressants are thought to increase prostaglandin synthesis and decrease water, sodium and potassium excretion. Secondary HTN – Sleep Apnea (OSA) Obstructive sleep apnea (OSA) is a sleep disorder that causes numerous pauses in breathing during sleep, as well as snoring and gasping for air. Many people do not know they have these symptoms. OSA is seen in 4 – 7% of the general population BUT it is found in 30-40% of patients with HTN. OSA causes overactivation o the SNS leading to increased heart rate and elevated BP. – Occurs every time a person’s airway collapses and briefly stops breathing – Also, when sleep is disrupted by OSA, the body releases stress hormones = Catecholamines (dopamine and epinephrine). Hypoxemia can also lead to oxidative stress, systemic inflammation and endothelium dysfunction, which all can lead to atherosclerotic cardiovascular disease. When there is narrowing of the pharynx, negative intra-thoracic pressure is generated and it increases the mechanical stress on the ventricles and atria, which can lead to left ventricle hypertrophy/atrial enlargement. OSA can also caused impaired baroreflex sensitivity which can lead to incorrect activation of the RAAS. Hypertension Low Blood Pressure JNC 8 Hypertension Guidelines *provided as reference Hypertension (HTN) Clinical impacts of HTN Arteries – vascular lining damage (atherosclerosis) Cerebral – effects of atherosclerosis result from carotid plaques that can occlude or embolize causing blindness from retinal infarction or ischemic stroke and disruption in the integrity of blood vessels in the brain (hemorrhagic stroke). Cardiac – effect from HTN can lead to concentric hypertrophy which can lead to fibrosis which can then lead to a stiff ventricle (*impaired diastolic filling) Renal – damages the kidneys and reduces its ability to manage blood pressure (*hypertensive nephrosclerosis) Hypertension Long term complications: – Heart failure (heart gets larger/weaker) – Aneurysms – Kidney failure – Heart attack – Ocular complications  Arteriosclerosis vs Atherosclerosis Both are conditions that affect the arteries, but they differ in their underlying causes and mechanisms. Arteriosclerosis Atherosclerosis General term for hardening and Is a specific type of arteriosclerosis. thickening of the arteries. Caused by buildup of fatty deposits Caused by: Age, HTN, DM and (plaque) on the inner walls of the smoking. arteries. Characterized by loss of elasticity and The deposits consists of cholesterol, flexibility in the arteries. calcium and other substances. Narrowing of the arteries occurs due to plaque buildup can restrict blood flow. Arteriosclerosis General term meaning “hardening of the arteries”. Can clinically manifest in different ways: – Coronary Artery Disease: buildup of plaque inside a coronary artery. – Peripheral Artery Disease: narrowing of the arteries in the legs, arms or pelvis. – Carotid Artery Disease: narrowing of the carotid arteries, which carry blood to the head and aorta. – Aortic Aneurysm: an abnormal enlargement in the aorta Arteriosclerosis There is a decrease in the elasticity of the arterial vessels occurs with age, which impair vessel function. Factors contributing to are increased collagen, reduced elastin and calcification. The arteries thicken/stiffen leading to an increase in BP. Treatment of Arteriosclerosis Treatment for arteriosclerosis includes a healthy diet, exercise, appropriate sleep (7-9 hr.s) stress management and smoking cessation. Medications can be used depending on the etiology: – BP medications to improve vessel function – Cholesterol medications to help with vascular diseases. – Aspirin to help reduce blood clot formation (81 milligrams) inhibits an enzyme called cyclooxygenase-1 (COX-1), which produces prostaglandins that promote platelet aggregation (sticking together). By blocking COX-1, aspirin reduces platelet aggregation, making it less likely for blood clots to form. Atherosclerosis Atherosclerosis is a chronic condition in which arteries harden through build-up of plaques. – Risk factors: dyslipidemia, diabetes, cigarette smoking, hypertension, and genetic abnormalities. – Main cause = hypercholesterolemia – Results in changes of the arterial endothelial permeability that allow the migration of lipids, especially LDL-C particles into the arterial wall. – Circulating monocytes adhere to the endothelial cells and acquire macrophage characteristics and engulf the LDL-C particles and convert into foamy macrophages (foam cells).  Atherosclerosis The foam cells eventually die and they get engulfed by nearby WBC’s and smooth muscle cells. This starts to form a plaque covered by the endothelial cells (atherosclerosis). Blood clots start to form on the damaged endothelial cells walls – Thrombus. Smaller particles can break off and clot vessels downstream (embolus) causing tissue ischemia. Treatment: Medications to manage Hyperlipidemia as well as Lifestyle modifications, increase physical activity, and smoking cessation. Statins – (HMG-CoA reductase Inhibitors) which inhibit the enzyme 3- hydroxy-3-methylglutaryl-coenzyme A. By blocking the enzyme production of cholesterol in the liver is reduced. Hypertension Vascular differences between the retina, the choroid, and the optic nerve allow for the different responses to hypertension. Hypertensive retinopathy – Often asymptomatic and presents bilaterally – It tends to present at a younger age and earlier in the overall systemic disease process in African-Americans. – 2nd most common retinal vascular disease – Prevalence = 4 – 10% Hypertension Initially see vasoconstriction – presence of vasospasm and an increase in retinal arteriolar tone. Clinically appears as generalized narrowing / attenuation of the retinal arterioles Hypertension – Persistent elevated blood pressure leads to intimal thickening, hyperplasia of the medial wall, and hyaline degeneration. Clinically correlates to more severe generalized and focal areas of arteriolar narrowing as well as alteration in the arteriolar light reflex. Gunn’s sign = A/V nicking Salus’ sign = venous deflection Bonnet’s sign = venous distal dilation Hypertension – Copper wiring When the arterioles become red-brown due to broadening/dimming of the light reflex due to increased thickness of the vessel wall. – Silver wiring Occurs when there is advanced sclerosis that leads to increased optical density of the retinal blood vessels – appears as sheathing of the blood vessels. Hypertension – Hypertensive Retinopathy Classification Original classification by Keith et al (Keith-Wagener- Barker) Scheie developed a classification scale that took into account arteriosclerotic changes. Keith-Wagener-Barker Grade Retinal Signs 1 Arteriolar attenuation 2 Grade 1 + AV crossing changes 3 Grade 2 + CWS, flame hemorrhages and exudates 4 Grade 3 + disc edema and macular star Scheie Grade Retinal Signs Arteriolar Sclerosis 0 No changes Normal 1 Barely detectable arteriolar Barely detectable light reflex narrowing changes 2 Obvious arteriolar narrowing Obvious increased light reflex with focal irregularities changes 3 Grade 2 + retinal Copper-wire arterioles hemorrhages and/or exudates 4 Grade 3 + papilledema Silver-wire arterioles Classification of Hypertensive Retinopathy on the Basis of Recent Population-Based Data (Wong & Mitchell) Grade of Retinal Signs Systemic Association Retinopathy None No detectable signs None Mild Generalized arteriolar narrowing, Modest association with risk focal arteriolar narrowing, AV nicking, of clinical stroke, subclinical opacity (“copper wiring”) or arteriolar stroke, coronary heart wall, or a combination of these disease, and death. signs. Moderate Hemorrhages, microaneurysm, CWS, Strong association with risk hard exudates, or a combination of of clinical stroke, subclinical these signs. stroke, cognitive decline, and death from cardiovascular causes. Malignant Signs of moderate retinopathy plus Strong association with swelling of the optic disc death Hypertensive Retinopathy Grade I and II are typically chronic Grade III and IV are typically acute findings Grade III or Moderate HTN Retinopathy – Diastolic blood pressure >= 110 Grade IV or Malignant HTN Retinopathy – Diastolic blood pressure >= 130mmhg Hypertension Referral – Grade I/II or Mild HTN Retinopathy Non-urgent referral – Grade III or Moderate HTN Retinopathy More urgent referral – Grade IV or Malignant HTN Retinopathy Immediate referral to ER Hypertension Other ocular conditions associated with Hypertension – CRVO/BRVO – CRAO/BRAO – Retinal artery macroaneurysm – Non-arteritic ischemic optic neuropathy (NAION) – Cranial Nerve Palsy Hypertension Hypertension Choroidopathy – More commonly found in the presence of malignant hypertension in younger patients. – Acute ischemic changes in the choriocapillaris and overlying RPE result in acute, focal RPE lesions. Hypertension Elschnig Spots – are changes in the RPE from non-perfused areas of the choriocapillaris. Siegrist Streaks – are linear hyperpigmented streaks over choroidal arteries, and they denote ischemia of the choroidal lobules. Typically seen in the temporal mid-periphery. Hypertension – Studies have shown that patients with Grade III/Moderate HTN Retinopathy had an increased risk of newly diagnosed clinical stroke (2–4x’s) – Studies also have shown that patients with Grade I / Mild HTN Retinopathy had a 2- 6x’s higher likelihood of having pre-existing coronary heart disease. Hypertension Treatment – Lifestyle changes Healthy diet Physical activity Healthy weight (BMI < 25) Managing stress Hypertension (HTN) Medications A–B–C–D A = angiotensin agents ACE inhibitors and Angiotensin receptor blockers (ARB’s) – Diminish the impact of dysregulated RAAS system on pressure elevation B = beta blockers – Reduce both cardiac output and vasoconstriction (peripheral resistance) Calcium channel blockers – Reverse vasoconstriction, reduction in cardiac output) Diuretics – Reduced plasma volume, possible reduction in peripheral resistance Hypertension (HTN) Other medications Alpha blockers / alpha-adrenergic antagonists – More common prescribed for impaired urinary flow in benign prostate hyperplasia. – Blocks stimulation of vascular smooth muscle, decreasing vascular resistance and lowering arterial blood pressure. – Due to reducing alpha stimulation it may cause orthostatic hypotension. – Due to increased incidence of CHF vs ACE inhibitors and diuretics Hypertension (HTN) Side effects of some of the medications – ACE inhibitors = chronic dry cough – ACE inhibitors &ARB’s = angioedema (swelling of lips, tongue, neck or face) – Beta blockers = fatigue, dry eyes, and sexual dysfunction – Calcium channel blockers = peripheral edema, headaches, and constipation – Diuretics = hypotension and dehydration are the most common QUESTIONS?