Pathophysiology Exam 2 (USM Nursing) – Flashcards

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Cilia
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● Hair like projections that extend from cell surfaces of lung epithelial cells. They propel mucous and trapped particles out of lower airway to be coughed out or swallowed
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Surfactant
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a lipoprotein produced by alveoli cells that has a detergent-like quality.produces surface tension on the alveoli, which enhances pulmonary compliance and prevents the alveoli from collapsing
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Diaphragm
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Dome shaped muscle that separates the thoracic and abdominal cavities. Diaphragm receives impulses that cause it to contract, lower and flatten which draws air into the lungs.
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Mediastinum
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the part of the thoracic cavity between the lungs that contains the heart and aorta and esophagus and trachea and thymus (but not lungs and pleura)
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Pleura
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Lung lining
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Hemothorax
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hemorrhage into pleural space
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Pneumothorax
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presence of air/gas in pleural space caused by rupture in visceral pleura or parietal pleura and chest wall.
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Empyema
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presence of pus in pleural space
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Atalactasis
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collapse of alveoli, surfactant inactivation
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Orthopnea
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dyspnea when a person is lying down
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COPD
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A combination of Emphysema and Chronic Bronchitis. COPD is irriversible, chronic hypercapnic shift. Leads to cor pulmonale & right sided HF.
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Emphysema
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Destruction of the alveolar walls leads to large, permanently inflated alveoli.Enzyme necessary for lung remodeling is deficient.Loss of elastic recoil and hyperinflation of the alveoli, leading to air trapping Manifestations: dyspnea upon exertion, diminished breath sounds, wheezing, chest tightness, tachypnea, hypoxia, hypercapnia, activity intolerance, anorexia, and malaise
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Chronic bronchitis
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Characterized by inflammation of the bronchi, a productive cough, and excessive mucus production Manifestations:hypoventilation, hypoxemia, cyanosis, hypercapnia, polycythemia, clubbing of fingers, dyspnea at rest, wheezing, edema, weight gain, malaise, chest pain, and fever
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Asthma
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Intermittent reversible airway obstruction. Acute airway inflammation, Bronchoconstriction, Bronchospasms, bronciole edema, mucous production Manifestations: wheezing, dyspnea, cough, anxiety, tachypnea, shortness of breath, chest tightness
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Manifestations of Pulmonary Embolism
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increase HR, increase RR, SOB, anxiety; pleural pain, hemoptysis, fever, increase WBC
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What causes Pulmonary Embolism
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Blood clot, 90% often from DVT Fats - femur fracture Air May infarct segment of lung, may cause sudden death Multiple small emboli (showers) - chronic or recurrent 2nd to cancer or clotting disorder
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How does O2 and CO2 exchange in the lungs? What process of movement is this called?
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In the capillary bed of the alveoli by passive diffusion
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Hypercapnia
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increase CO2 levels
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Hypocapnia
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decrease CO2 levels
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Hypoxia
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decreased O2 levels in tissue and cells
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Hypoxemia
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decreased O2 levels in the blood
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ARDS
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(Acute Respiratory Distress Syndrome) Hyperventilation, Respiratory alkalosis, Dyspnea and hypoxemia, Metabolic acidosis, Hypoventilation, Respiratory acidosis, Further hypoxemia, Hypotension, decreased cardiac output, death ○ PaO2 less than 50 mm Hg ○ PaCO2 greater than 50 mm Hg ○ pH less than 7.25
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What causes ARDS?
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Occurs in response to other condition:Sepsis,fluid overload,shock, burns, DIC,aspiration,neurologic injuries Massive pulmonary inflammation Damage to the alveolocapillary membrane pulmonary edema, decreased lung compliance, impaired alveolar ventilation Surfactant inactivation - Atelectasis
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What are manifestations of ARDS?
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labored/shallow respirations, rales, productive cough w/ frothy sputum, hypoxia, caynosis, tachycardia
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Cor pulmonale
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Pulmonary heart disease causesRight ventricular enlargement Secondary to pulmonary hypertension Pulmonary hypertension creates chronic pressure overload in the right ventricle leading to right sided HF
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What are the clinical manifestations of cor pulmonale
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Exertion dyspnea Fatigue and weakness Jugular vein distention, hepatosplenomegaly, peripheral edema Abnormal ECG showing right ventricular hypertrophy
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Community acquired pneumonia
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Streptococcus pneumoniae— most common Mycoplasma pneumoniae—common in adolescents Influenza virus—most common viral in adults
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Hospital acquired pneumonia
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Pseudomonas aeruginosa Staphylococcus aureus
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Pneumonia associated w/ HIV/AIDS
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Pneumocystis jiroveci (formerly carinii)
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Clinical manifestations of lung cancer
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persistent cough(chronic over 2-3 weeks) or a change in usual cough, dyspnea, hemoptysis, frequent respiratory infections, chest pain, hoarseness, weight loss, anemia, fatigue, and other symptoms specific to site of metastasis
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Pathophysiology of TB
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1. Primary infection:bacillus enters body, some travel to lymph nodes, activates type IV hypersensitivity, lymphocytes/macrophages for a granuloma, tubercle, caseous necrotic tissue, in healthy people become calcified (Ghon Complexes) but can remain dormant 2. Secondary/ Active infection: TB spreads in lungs/other organs
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Manifestations of TB
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productive cough, hemoptysis, night sweats, unexplained weight loss, fever/chills, anorexia
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What allows TB to lie dormant?
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Scar tissue around tubercle - tubercles form and become scar tissue (caseous necrosis) after 10 days, becomes dormant but not dead for life. Reactivated by malnutrition, type 1 diabetes, immunocompromise.
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Manifestations of chronic hypoxia
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clubbing, polycythemia, cor pulmonale, prolonged hypercapnia
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Review ABG values
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PaCO2= 35-45 HCO3= 22-26 PH= 7.35-7.45 PaO2=80-100
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Describe cardiovascular circulation
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Superior/Inferior Vena Cava, RA, Tricuspid, RV, Pulmonary Valve, Pulmonary Artery, Lungs, Pulmonary Vein, LA, Mitral, LV, Aortic Valve, Aorta, Body
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Vessels of the Coronary Arteries
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Right Coronary Artery, Right Marginal, Anterior Intraventricular Artery, Posterior Intraventricular Artery, Left Coronary Artery, Left Circumflex Great Cardiac Vein, Middle Cardiac Vein, Small Cardiac vein
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Where is the opening of the Coronary Arteries?
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Coronary ostea
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Where do Coronary veins drain into?
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Coronary sinus in the RA
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Describe the conduction of a healthy heart
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SA Node, Atrial Contraction, AV Node, Bundle of His, L/R bundles, Perkenji fibers, Ventricular contraction
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What is the primary pacemaker?
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Sinal Atrial (SA) Node 60-100 bpm
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What are the back up pacemaker?
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Atrial Ventricular (AV) Node 40-60 bpm Bundle branches/Perkenji Fibers <40 bpm
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Describe pericarditis
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● Pericarditis- inflammation of the pericardium. ○ Fluid accumulates called pericardial effusion, swollen tissue creates friction. ● Constrictive pericarditis- loss of elasticity, results from chronic inflammation
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Clinical manifestation of pericarditis
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pericardial friction rub, sharp sudden , severe chest pain that increases with deep inspiration and decreases when sitting up and leaning forward, dyspnea, tachycardia, edema, flulike symptoms
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Describe cardiac temponade
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cardiac compression from excessive fluid accumulation. Life threatening
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Clinical manifestations of cardiac temponade
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arterial pressures fall, rising venous pressures, narrowing pulse pressure, and muffled heart sounds. Comp- heart failure, shock, and death
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What causes Dilated Cardiomyopathy?
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Caused by ischemic heart disease and hypertension, infections, toxins, connective tissue disease, nutritional deficiencies, idiopathic results from extensively damaged myocardium fibers
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What causes hypertrophic Cardiomyopathy?
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Diastolic dysfunction, hypertrophic ventricle becomes stiff leading to decreased ventricular filling. leading to decreased CO
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Manifestations of Dilated Cardiomyopathy
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Dyspnea, non productive cough, orthopnea, paroxysmal nocturnal dyspnea, dysrhythmias, angina, dizziness, activity intolerance, jugular vein distention, murmurs, peripheral edema, poor cap refill, Hepatomegaly
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Manifestations of Hypertrophic Cardiomyopathy
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Syncope, left ventricular failure, infarction (similar to dilated)
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Patho and Manifestations of Aortic Stenosis and problems it causes
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Aortic Stenosis:→hypertrophy of left ventricle→blood backs into left atrium→AFIB→blood back up into pulmonary circulation→pulmonary edema, leads to left sided heart failure Manifestations: murmur, angina, syncope, pulmonary edema, dyspnea on exertion
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Patho and Manifestations of Mitral Stenosis and problems it causes
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Mitral Stenosis:→hypertrophy of left atrium→blood backs up into pulmonary circulation→pulmonary edema, leads to left sided heart failure Manifestations:similar to aortic, dysrhythmias, decreased cardiac output, pulmonary hypertension, orthopnea, increased respiratory infections.
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What is Rheumatic heart disease?
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Valvular damage: inflammation, erosion, and deposition of clumps of vegetation.Myocarditis and pericarditis can also occur.
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What causes Rheumatic heart disease?
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Type II reaction. Group A beta hemolytic strep. Not the strep itself but body's response to the strep that causes the problem. 10% of patients with untreated rheumatic fever will develop RHD.
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Infective endocarditis and 3 steps of progression
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○ Infection by Streptococcus viridans and Staphylococcus aureus infections ○ Vegetation forms on internal structures and creates small thrombi ○ Microemboli occur as they are dislodged, resulting in microhemmorages
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Risk factors for Infective endocarditis
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valvular heart disease, prosthetic valves, long term indwelling catheters, IV drug use, dental procedures, recent cardiac surgery
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What are the clinical manifestations of infective endocarditis
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flu like symptoms, splinter hemorrhage under nails, Osler's nodes, petechiae, Hematuria
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Describe heart failure
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congestive heart failure, blood cannot pump adequate amount of blood to meet the body's needs
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Manifestations of Left Sided HF
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pulmonary congestion (rales), orthopnea
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Manifestations of Right Sided HF
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weight gain, edema, distended jugular veins, cor pulmonale (systemic effects)
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Preload
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how much blood is coming into heart and the stretch against ventricles because of that blood Frank Starling Law= greater volume, greater pressure, better contractility until a point and then it starts to lose contractility over time
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Afterload
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force the heart is working against, resistance
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Stroke Volume
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effected by preload, afterload and contractility
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Cardiac output
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Amount of blood pumped every minute Stroke Volume X HR=CO 4-8 L per minute
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Cardiogenic shock
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Failure of heart pump, something happened at heart level- left ventricle cannot maintain adequate cardiac output. Compensatory mechanisms of heart failure are triggered;however these mechanisms increase cardiac workload and O2 consumption, resulting in decreased contractility. Tissue and organ perfusion decreases, leading to multi-system organ failure
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Nuerogenic shock
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decrease in sympathetic tone in vascular smooth muscle leads to massive vasodilation
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Septic shock
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caused by bacterial infection (septicemia)
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Anaphylactic shock
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Hypersensitive reaction to an allergen
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Hypovolemic shock
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Venous return reduces because of external blood volume losses. Preload drops decreasing ventricular filling and stroke volume. As cardiac output falls, tissue and organ perfusion decreases.
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Common steps for all forms of shock
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1.activation of compensatory mechanisms such as the SNS and RAA 2. compensatory mechanisms fail to maintain CO, cells use anaerobic respiration, lactic acid builds up, metabolic acidosis, sluggish blood flow, increased coagulation 3. irreversible shock leading to irrerversible organ damage and cardiac failure
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What does the P wave represent on an EKG
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Atrial Depolarization
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What does the QRS complex represent on an EKG
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Ventricle Depolarization
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What does the T wave on represent on an EKG
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Ventricle Repolarization
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Automaticity
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cell's ability to generate electrical impulse (generate own impulse)
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Refractoriness
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rest before another impulse
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Excitability
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The ability to respond to stimuli by the production of electrical impulses
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Conductivity
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ability to transmit an impulse from cell to cell
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What occurs during Diastole
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relaxation of ventricles- ventricles fill
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What occurs during Systole
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contraction of ventricles- blood is pushed out of ventricles
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Describe the steps in the development of atherosclerosis.
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Chronic inflammatory disease characterized by thickening and hardening of the arterial wall. Triggered by a vessel wall injury. Lesions develop on vessel wall and calcify over time. Leads to vessel obstruction, platelet aggregation, and vasoconstriction
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List the risk factors for the development of primary hypertension
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Age, Race, Overweight/Obese, Sedentary, Tobacco use, high Sodium diet, low Potassium diet, high Vitamin D, Alcohol, Stress, Chronic conditions (dyslepedemia, diabetes, renal disease, sleep apnea)
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List complications that may occur from hypertension.
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atherosclerosis, aneurysms, HF, Stroke, Hypertensive crisis, Renal damage, Vision loss, Metabolic syndrome, Problems w/ memory and understanding
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What is orthostatic hypotension? What are the causes?
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Decrease in both systolic and diastolic blood pressure upon standing Sluggish blood pressure compensation in response to (baroreceptor) gravitational changes on the circulation Causes: Medications, Dehydration, Physical exhaustion Venous pooling (pregnancy, extensive varicosities)
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What is an embolus? Thrombus?
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● Thrombus- stationary blood clot ● Embolus- traveling body. Floats through blood. May be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and foreign substances. Can become lodged in places like the lungs, brain, and heart
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Describe the different types of aneurysm.
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○ saccular aneurysm- bulge on the side ○ fusiform- occurs the entire circumference Atherosclerosis is the most common cause, hypertension is a contributing factor
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What is a true aneurysm?
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affects all 3 vessel layers.
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Describe Raynaud phenomenon and disease, think about the causes, processes and symptoms
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result of vasospasms of arteries, most often of the hands, that occur because of sympathetic stimulation. Raynaud's phenomenon describes when these vasospasms occur with an autoimmune disease (systemic lupus erythema and scleroderma). As vessel occlusion increases, the ischemia to the affected tissue becomes worse.
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What are clinical manifestations of chronic venous insufficiency?
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DVT- Virchow's Triad o Venous stasis o Venous endothelial damage o Hypercoagulable state Vericose Veins:dilated, tortuous, engorged veins (vericose veins) Manifestations: Irregular, purplish, bulging veins,Pedal edema, Fatigue,cAching in the legs, Shiny, pigmented, hairless skin on the legs and feet-Skin ulcer formation
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What is stable angina? What causes it? How is it different from unstable angina.
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ischemia that is initiated by increased demand (activity) and relieved with the reduction of that demand (rest) Caused by reduction of O2 to the cardiac muscles that produces chest pain Unstable angina is unpredictable, pre-infarction stage
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What lab values are monitored to confirm the diagnosis of myocardial infarction (MI)?
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● Cardiac troponins (troponin I and troponin T) are most specific for MI (these are enzymes released when heart muscle damaged) ○ creatine kinase (released w/any type of muscle damage ○ lactic dehydrogenase
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What is hematopoiesis and where does it occur?
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the production of blood cells, takes place in the spleen and liver of a fetus and in the bone marrow after birth.
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What is a stem cell?
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Stem cells (primitive cells) differentiate the precursors for the different blood cells. All blood cells come from one pluripotent stem cell. Can branch into Myologenic/Lymphactic
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What are erythropoietin and thrombopoietin, where do they come from and what do they do?
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erythropoietin- hormone produced by the kidneys that stimulates production of RBCs in bone marrow thrombopoietin- hormone produced by the kidneys that stimulates the production of platelets in bone marrow
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Describe the functions of the spleen and lymph nodes
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Spleen: Filters and cleans blood, mounts immune response against blood-borne pathogens, serves as blood reservoir Lymph nodes - Part of the immune and hematologic systems ● Facilitates maturation of lymphocytes ● Transports lymphatic fluid back to the circulation ● Cleanses the lymphatic fluid of microorganisms and foreign particles
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What is a normal platelet count?
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● Normal Value: 150,000-400,000/mm3 ● <50,000/mm3: hemorrhage from minor trauma (anything uner 100,000 should not be on asprin or any other kind of blood thinner) ● <15,000/mm3: spontaneous bleeding ● <10,000/mm3: severe bleeding
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What is the role of platelets in hemostasis?
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Forms platelet plug Thrombin + Fibrinogen= fibrin
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What other processes and substances participate in hemostasis?
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1. Vessel spasm 2. Formation of platelet plug 3. Blood coagulation 4. Clot retraction 5. Clot dissolution
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What is polycythemia vera? What are the clinical manifestations?
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Abnormally high erythrocytes,Considered a neoplastic disease Increased blood volume and viscosity, leading to tissue ischemia and necrosis Manifestations:cyanotic or plethoric skin, high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities
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Know the normal WBC count.
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● White blood cells -normal level is 5,000 to 10000 mm3
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List the WBCs, identify which are granulocytes and agranulocytes, describe their function
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● Granulocytes ○ Neutrophils - small phagocyte ○ Eosinophil- ○ Basophil-histamine ● Agranulocytes ○ Monocytes/Macrophages - phagocytize bacteria ○ Lymphocyte -involved in immune protection
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What is the cause of infectious mononucleosis? Which cells are infected?
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● Cause: Epstein Barr Virus ● Infects B cells by killing the cell or being incorporated into genome
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Describe multiple myeloma
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(plasma cell) B cell cancer, malignant plasma cells, chromosomal break, plasma cells infiltrate bone and organs. ii. Anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain,
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Describe Leukemia
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Cancer of the leukocytes Leukemia cells abnormally proliferate, crowding normal blood cells
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Differentiate between the different types of leukemia
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a. Acute lymphocytic (ALL) b. Acute myelogenous (AML) c. Chronic lymphocytic (CLL) d. Chronic myelogenous (CML
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contractility
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mechanical response, how well the heart contracts
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What causes cool/clammy skin in shock pts
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Vasoconstriction/shunting of blood to vital organs
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ITP (Idiopathic Thrombocytopenia Purpura)
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○ causes: idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections ■ Hypocoagulation resulting from an autoimmune destruction of platelets ○ clinical manifestations:bleeding or indications of bleeding (e.g. bruising, petechia, etc)
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DIC (
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○ causes: Life-threatening complications of many conditions, Results from an inappropriate immune response ■ Widespread coagulation followed by massive bleeding because of the depletion of clotting factors ○ clinical manifestations: tissue ischemia and bleeding
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TTP (Thrombotic Thrombocytopenia Purpura)
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○ causes: idiopathic causes, heredity, bone marrow transplants, cancer, medications, pregnancy, and HIV ■ Deficiency of enzyme necessary for cleaving von Willebrand's factor, leading to hypercoagulation ■ Hypercoagulation depletes platelet levels ○ clinical manifestations:purpura, changes in consciousness, confusion, fatigue, fever, headache, tachycardia, pallor, dyspnea on exertion, speech changes, weakness, and jaundice
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Pernicious Anemia (Macrocytic Normochromic)
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● Cause: B12 deficiency caused by lack of instrinsic factor ● Manifestations:•bleeding gums, diarrhea, impaired smell, loss of deep tendon reflexes, anorexia, personality or memory changes, positive Babinski's sign, stomatitis, paresthesia, and unsteady gait
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Iron Deficiency Anemia (Mycrocytic Hypochromic)
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● Cause: inadequate intake, inadequate absorption, increased bleeding ● Manifestations: cyanosis to sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, pica, and delayed healing
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Aplastic Anemia (Normocytic Normochromic)
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● Cause: insidious, autoimmune, medications, medical treatments, viruses, and genetic ● Manifestations:-Anemia (e.g., weakness, pallor, dyspnea)-Leukocytopenia (e.g., recurrent infections)-Thrombocytopenia (e.g., bleeding)
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cricoid cartilage
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