Pathophysiology Week 3 Study Guide PDF

Week 3 Chapter 16 Define primary and secondary hypertension o Primary Hypertension ▪ Idiopathic disorder, meaning that there is no direct cause of hypertension ▪ Primary hypertension is the most common form of hypertension ▪ Pr...

Week 3 Chapter 16 Define primary and secondary hypertension o Primary Hypertension ▪ Idiopathic disorder, meaning that there is no direct cause of hypertension ▪ Primary hypertension is the most common form of hypertension ▪ Primary hypertension is rare for patients under the age of 10 years old ▪ There are three subtypes of primary hypertension: Isolated systolic hypertension – A heightened systolic blood pressure when diastolic blood pressure remains stable and constant Isolated diastolic hypertension – A heightened diastolic blood pressure when systolic blood pressure remains stable and constant Combined systolic and diastolic hypertension – An overall increase in blood pressure, where both systolic and diastolic pressures are elevated ▪ Systolic hypertension is a major risk factor for cardiovascular diseases ▪ Risk factors of primary hypertension Nonmodifiable risk factors are: o Age o Family history Modifiable risk factors are: o Diet o Sedentary lifestyle o Obesity o Metabolic syndrome, where metabolic syndrome describes the majority of other factors where the body is impacted, causing high blood pressure ▪ Primary hypertension can lead to end-organ damage in the following organs: Heart – increased myocardial workload causing heart failure Kidneys – Glomerular damage causing kidney failure Eyes – Affects microcirculation of the eye Brain – Increases cerebral vasculature blood pressure causing hemorrhage o Secondary Hypertension ▪ Identifiable pathology or condition that causes hypertension ▪ Most common in children under the age of 10 years that have some type of condition associated ▪ Can be related to the following conditions: Renal disease Coarctation of the heart (congenital defect where the aorta is narrower than normal) Pregnancy Obesity Sleep apnea  Endocrine disorders Hypertensive urgency vs. emergency (crisis) o Hypertensive urgency is the least severe of the two listed here o Hypertensive urgency is defined as sudden increase in either systolic or diastolic blood pressure without the evidence of end-organ damage ▪ Usually can be controlled with medications over 24 to 48 hours o Hypertensive emergency is defined as sudden increase in either systolic or diastolic blood pressure with evidence of end-organ damage ▪ Hypertensive emergencies must be controlled and usually occur in ICU settings Symptoms of hypotension (dizziness, blurred vision, confusion, and syncope) o Symptoms of hypotension include: ▪ Dizziness ▪ Lightheadedness ▪ Weakness ▪ Fatigue ▪ Blurred vision ▪ Confusion ▪ Fainting or syncope ▪ Confusion ▪ Difficulty concentrating ▪ Tachycardia End organ damage of hypertension o End organ damage is the impairment or damage of major organs of the body due to the effects of hypertension o This can manifest as the following: ▪ In the vascular system: Endothelial dysfunction Remodeling of arteries Atherosclerosis Arteriosclerotic stenosis Aortic aneurysm ▪ In the brain: Stroke Hemorrhage Retinopathy ▪ In the heart: Left ventricle hypertrophy Chronic heart failure Myocardial infarction Heart failure ▪ In the kidneys: Albuminuria Proteinuria Chronic renal insufficiency  Renal failure Understand how modifiable risk factors are the first and most important intervention in managing hypertension (case scenario question) o Modifiable risk factors are the highest contributing factors to hypertension, where the majority of hypertensive manifestations can be managed or removed by lifestyle changes by the patient o Modifiable risk factors include: ▪ A poor diet high in fat, which increases LDL cholesterol, leading to atherosclerosis ▪ Sedentary lifestyle leads to weakening of the body’s vasculature and heart ▪ Obesity ▪ Metabolic syndromes ▪ Lifestyle modifications to reduce modifiable risk factors include: Weight reduction DASH Diet (Dietary Approaches to Stop Hypertension) Decrease of sodium intake Reduction of alcohol intake Know Blood Pressure Classification ranges (normal, prehypertension, Stage 1, Stage 2) table 16.2 o Normal Range: < 120 / < 80 mmHg o Prehypertension: 120 – 140 / 80 – 89 mmHg o Stage 1 Hypertension: 140 – 159 / 90 – 99 mmHg o Stage 2 Hypertension: > 160 / > 100 mmHg The importance of sodium in hypertension o When low blood pressure is detected by baroreceptors in the kidneys, the RAAS cycle is initiated. At the end of the RAAS cycle, aldosterone introduces channels into the kidneys, where sodium is retained instead of secreted. Wherever sodium travels, water also travels. This is intended to increase the body volume, which in turn increases the blood volume, which in turn increases blood pressure. Consuming too much sodium, which means that it is consumed higher than the rate that it is secreted from the body, leads to higher sodium content in the blood, meaning higher water content in the blood, thus increasing blood pressure higher than anticipated. There are no real good physiological mechanisms for lowering blood pressure directly, so chronic consumption of sodium leads to chronic elevation of blood pressure. The action of an ACE inhibitors o ACE inhibitors are used to prevent the RAAS process from completing, which increases blood volume, which then increases body volume, which increases blood pressure. ACE inhibitors prevent angiotensin I converting enzyme (ACE) from converting angiotensin I to angiotensin II. This prevents vasodilation and release of aldosterone from the adrenal glands, thereby causing vasodilation of blood vessels and less retention of sodium and water collected during renal processing. Complications of orthostatic hypotension (stroke, cognitive impairment, and death) o Orthostatic hypotension is low blood pressure due to physical body position o This is usually categorized by a 20 mmHg drop in blood pressure, or a 10 mm Hg drop in blood pressure within 3 minutes  o Hypotension is characterized by an excessive increase in heart rate o Causes of hypotension are: ▪ Vasomotor or baroreceptor response issues ▪ Drug therapy adverse effects ▪ Arterial stiffness ▪ Blood volume depletion ▪ As a result of a secondary disease process Chapter 18 Pulmonary stenosis o Pulmonary stenosis is the abnormal fusion of the valvular cusps that can lead to right ventricular hypertrophy o The pulmonary valve controls the blood flow from the right ventricle into the pulmonary artery o When there is narrowing of the pulmonary valve, the right ventricle must work much harder to move the same volume of blood per heart contraction, leading to right ventricular hypertrophy The correlation of LDL levels and coronary artery disease o High-density lipoproteins (HDL) are easily broken down in the liver and are easy to manipulate and metabolize. Low-density lipoproteins (LDL) are not easily broken down, and therefore, spend more time in the blood stream o The structure of an LDL protein is jagged and sharp, so with an increase in LDL proteins in the blood, there is a higher instance and opportunity for LDL proteins to damage epithelial cells in the vasculature of the body o When an epithelial cell is damaged by LDL, there is an inflammatory and immune response, and endothelial cells become permeable, recruiting leukocytes o This mechanism traps the LDL protein in the cell wall and is called LDL insudation o Endothelial cells and macrophages begin oxidizing the lipid, which damage endothelial cells and smooth muscle cells, bringing more macrophages to the area o Macrophages engulf the LDL protein and foam cells are formed ▪ A foam cell is a lipid-filled macrophage o These foam cells release inflammatory mediators and growth factors, causing formation of more muscle tissue, forming a lipid core o Over time, more lipids and blood debris collect on this foam cell, forming a thrombus, which contributes to narrowing of the artery, which is indicative of coronary artery disease Stable angina vs. Unstable angina o Stable angina ▪ Stable angina is defined as chest pain that occurs as a result of predictable actions, such as exertion or stress, and is usually relieved by rest or administration of nitroglycerin ▪ Stable angina is the most common form of angina, also called classic angina  ▪ Stable angina is usually caused by a large, stable atherosclerotic plaque that causes chronic occlusion of a coronary vessel o Unstable angina ▪ Unstable angina is defined as unpredictable attacks of chest pain that is unrelated to physical or emotional exertion, heart rate, or other obvious causes where myocardial oxygen demand is increased ▪ Unstable angina is also called prinzmetal or variant angina ▪ Unstable angina is characterized by the following: Vasospasms Atherosclerosis-induced hypercontractility Abnormal secretion of vasospastic chemicals from mast cells Abnormal calcium flux across vascular smooth muscle ▪ Unstable angina can lead to coronary ischemia Complications of Acute coronary syndrome (NSTEMI, STEMI) o A STEMI is an ST-Elevated Myocardial Infarction ▪ A STEMI is detected by an electrocardiogram ▪ Symptoms of a STEMI involve chest pain and evidence of acute ischemia as demonstrated on the ECG o A non-STEMI is a non-ST-Elevated Myocardial Infarction ▪ A non-STEMI is not easily detected on an ECG because there is no ST-segment elevation ▪ Symptoms of a STEMI involve chest pain, presented as unstable angina o The main difference between a STEMI and a non-STEMI is that a STEMI shows on an ECG and a non-STEMI does not and symptoms are worse that do not resolve with rest or are easily induced o Complications of Acute Coronary Syndrome are: ▪ Heart failure ▪ Myocardial infarction due to complete occlusion Ultimate size of myocardial tissue death depends on the extent, duration, and severity of the ischemia ▪ Stroke due to embolus formation ▪ Arrhythmias ▪ Cardiogenic shock ▪ Acute kidney failure ▪ Dressler syndrome Diagnostic tests and findings to detect Myocardial Infarction (MI) o Diagnostic tests for detection of myocardial infarctions involve the following: ▪ Analysis of signs and symptoms ▪ Tests like myoglobin, troponin, lactate dehydrogenase, creatinine kinase The test of choice for MI is troponin, because it is the only indicator of damage to specifically cardiac muscle tissue ▪ Electrocardiogram changes ST-segment elevation Large Q waves  Inverted T waves Rheumatic heart disease o Rheumatic heart disease is an acute inflammatory disease that is caused by a beta- hemolytic streptococci bacterial infection o Antibodies against streptococcal antigens affect the connective tissue in the joints, the heart, and the skin o Rheumatic disease mainly occurs in children o Symptoms of rheumatic heart disease include: ▪ Fever ▪ Sore throat ▪ Joint inflammation ▪ Involuntary movement ▪ Distinctive truncal rash Describe the different congenital heart defects (Example: patent ductus arteriosus) o Atrial Septal Defect ▪ Defect along the foramen ovale, which is an unexpected opening between the left atrium and right atrium that is expected to close after birth ▪ Patients with atrial septal defect have excess blood returning back to the lungs, causing an increase in pulmonary artery pressure and prevents delivery of oxygenated blood to the body ▪ Can lead to pulmonary hypertension, right ventricular hypertrophy, and a right- to-left shunt, which means that blood moves from the right atrium to the left atrium, which means deoxygenated blood gets delivered to the body Right to left shunt can cause cyanosis because deoxygenated blood is circulating o Ventricular Septal Defect ▪ Defect along the membranous septum by the bundle of His, and an unexpected opening is found between the left ventricle and the right ventricle ▪ Patients with ventricular septal defect have excess blood returning back to the lungs, causing an increase in pulmonary artery pressure and prevents delivery of oxygenated blood to the body ▪ Can lead to pulmonary hypertension, right ventricular hypertrophy, and a right- to-left shunt o Patent Ductus Arteriosus ▪ Defect of the patent ductus arteriosus, which is supposed to close after birth, but does not ▪ Patients with a patent ductus arteriosus have excess blood returning back to the lungs, causing an increase in pulmonary artery pressure and prevents delivery of oxygenated blood to the body ▪ Can lead to pulmonary hypertension, right-sided heart failure o Coarctation of the Aorta ▪ Defect of unusual narrowing of the aorta that impedes blood flow ▪ Is commonly located before or after the ductus arteriosus  ▪ Characterized by upper extremities having an increased blood pressure and the lower extremities having a low blood pressure and a weak pulse ▪ Can lead to ventricular hypertrophy and systolic murmurs o Tricuspid Atresia ▪ Defect characterized by an underdeveloped or malformed tricuspid valve ▪ Tricuspid atresia is usually associated with an underdeveloped right ventricle and an atrial septal defect, allowing blood to flow ▪ Surgery is required for survival o Pulmonary Stenosis or Pulmonary Atresia ▪ Pulmonary Atresia: Defect characterized the path of blood having to travel through a septal opening to the lungs instead of through the pulmonary artery ▪ Pulmonary stenosis Defect characterized by abnormal fusion of valvular cusps ▪ Can lead to right ventricular hypertrophy o Aortic Stenosis or Aortic Atresia ▪ Aortic Stenosis: Defect characterized by valvular cuffs or the subvalvular fibrous ring being malformed or misshapen ▪ Can cause high ventricular afterload and left ventricular hypertrophy ▪ Aortic Atresia: Not compatible with survival due to blockage of blood flow to the body o Tetralogy of Fallot is a cyanotic congenital defect characterized by the following: ▪ Ventricular septal defect ▪ Aorta positioned above the ventricular septal opening ▪ Pulmonary stenosis ▪ Right ventricular hypertrophy o Transposition of Great Arteries ▪ Transposition of the great arteries replaces the aorta with the pulmonary artery and the pulmonary artery with the aorta, resulting in noncommunicating circulations ▪ Mixing of blood occurs and this is not compatible with survival o Truncus Arteriosus ▪ Defect characterized by lack of separation of the pulmonary artery and the aorta to separate, which means that blood is received from both the left ventricle and right ventricle ▪ Can cause pulmonary hypertension and right ventricular hypertrophy Chapter 19 Symptoms of right and left sided heart failure o Left Sided Heart Failure ▪ Backward Effects Dyspnea on exertion  Orthopenia Cough Paroxysmal nocturnal dyspnea Cyanosis Basilar crackles ▪ Forward Effects Fatigue Oligouria Increased Heart Rate Faint Pulse Restlessness Confusion Anxiety o Right Sided Heart Failure ▪ Backward Effects Hepatomegaly Ascites Splenomegaly Anorexia Subcutaneous Edema Jugular Vein Distension ▪ Forward Effects Fatigue Oliguria Increased Heart Rate Faint pulse Restlessness Confusion Anxiety Know the term paroxysmal nocturnal dyspnea Reduced cardiac output in heart failure Complications of dysrhythmias (Indicates an underlying condition and can impair cardiac output.) o There are three types of arrhythmias ▪ Abnormal sinus rhythm ▪ Abnormal site of impulse initiation ▪ Disturbances in conduction pathways o Arrhythmias lead to two complications: ▪ Indication of underlying pathophysiologic disorder ▪ Impairment of normal cardiac output o Types of complications ▪ Sinus tachycardia Increased demand for cardiac output and reduced stroke volume ▪ Sinus bradycardia  Low heart rate precipitates a low cardiac output ▪ Sinus arrhythmia No complications known and is normal ▪ Sinus arrest Absence of impulse initiation and results in the heart stopping ▪ Atrial flutter and fibrillation Can cause thrombus formation and lead to ischemia ▪ Ventricular dysrhythmia Compromises cardiac output ▪ Ventricular tachycardia ▪ May be fatal of nor rapidly managed ▪ Ventricular fibrillation ▪ Results in death if not reversed within minutes Cardiac tamponade o Cardiac tamponade is the buildup of fluid in the pericardium that causes pressure on the heart, resulting in improper pumping of blood due to compression from an external force o Cardiac tamponade leads to decreased cardiac output and shock if not treated promptly Cor Pulmonale (Primary right-sided HF due to a primary pulmonary condition) o Cor pulmonale is a condition where the right side of the heart becomes enlarged and weakened due to specifically underlying lung diseases such as pulmonary embolism or pulmonary hypertension as a cause o Pulmonary condition>Increased pulmonary vascular resistance>pulmonary hypertension>right sided HF Chapter 20 Signs, symptoms, risk factors, and pathogenesis of anaphylactic shock o Anaphylactic shock is a type of distributive shock, characterized by excessive vasodilation and peripheral blood pooling o Cardiac output is inadequate because of reduced preload o Anaphylactic shock is a result of mast cells degranulating as a result of IgE antibody mediation o Mast cells release large amounts of vasodilatory mediators, resulting in hypotension o Causes of anaphylactic shock are: ▪ Antibiotic therapy Beta-lactam antibiotics particularly ▪ Peanuts and tree nuts ▪ Insect stings ▪ Snake bites o Symptoms of anaphylactic shock are: ▪ Urticaria ▪ Bronchoconstriction ▪ Stridor  ▪ Angioedema ▪ Wheezing ▪ Itching Define sepsis and septic shock o Septic shock is the systemic inflammatory response o an infection o Causes are usually gram-negative and gram-positive bacteria and fungal infections o Septic shock initiation triggers the clotting cascade, the complement system, and the kinin system, which leads to significant vasodilation, hypotension, maldistribution of blood flow, cellular hypoxia, and edema formation o Septic shock can have a high cardiac output with warm extremities that still experiences cellular hypoxia, which then deteriorates to a hypodynamic phase ▪ The hypodynamic phase has a decreased cardiac output and leads to organ ischemia Types of obstructive shock Box 20.1 o Pulmonary embolism o Cardiac tamponade o Tension pneumothorax o Dissecting aortic aneurysm Cardiogenic shock o Cardiogenic shock is the result of severe ventricular dysfunction associated with myocardial infarction o Diagnostic features include: o Decreased cardiac output o Elevated left ventricular end-diastolic pressure (preload) o S3 heart sounds o Pulmonary edema