NURS 8022 Advanced Pathophysiology Exam 3 Study Guide Latest Update | Rated A+, Exams of Nursing

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NURS 8022 Advanced Pathophysiology Exam 3 Study Guide Latest Update | Rated A+ Exam #3 Study Guide Respiratory Structures of pulmonary system – NOT ON STUDY GUIDE • Lobes (3 on right, 2 on left) - segments – lobules • Blood vessels serve the pulmonary system • Chest wall/thoracic cage • Diaphragm: involved in ventilation – dome shaped muscle that separates the thoracic and abdominal cavities • Mediastinum: space between lungs containing heart, great vessels, and esophagus • Conductingairways o Upperairways: warms and humifies air § Nasopharynx and oropharynx o Larynx: connects upper and lower airways o Lowerairways § Trachea, bronchi, terminal bronchioles • Carina: ridge where the tracheadivides into the right and left bronchi • Hila: where the right and left bronchi enterthe lungs, along with blood and lymph vessels • Goblet cells: produce mucus • Cilia: hair-like structures – work with goblet cells to propelforeign material up and enable it to be coughed up • Pleura: serous membrane – adheres firmly to the lungs and folds overitself o Visceral: coveringthe lungs; Parietal: lining the thoracic cavity o Pleural space: fluid lubricates the pleural surfaces allowing them to slide overeach other § Pressure in pleural space: negative (-4 to –10); keeps lungs from collapsing § Inspiration – chest cage pulled outward on lungs creates greaternegative pressure Understand basic structure and function of alveoli • Gas exchange airways: acinus - “berry” o Respiratory bronchioles o Alveolar ducts o Alveoli § Primary gas exchange units § Oxygen enters the blood and carbon dioxide is removed § Epithelial cells • Type 1 alveolar cells: provide alveolar structure • Type 2 alveolar cells: surfactant production – prevents lung collapse § Contain alveolar macrophages: ingest foreign materialand remove it through lymphatic system Surfactant – its function and where it comes from • Detergent like substance secreted by type 2 alveolar epithelial cells in lungs • Keeps alveoliopen and free of fluid and pathogens (collectins) • Decrease surface tension by blocking H20 and H+ binding in alveolar space – prevents collapse – allow airflow in more easily Understand the mechanics of the pulmonary circulation and how it relates to systemiccirculation • Pulmonary circulation functions: • Peripheral chemoreceptors o Located in the aorta and carotid bodies o Stimulated by hypoxia (PaO2) o Responsible forall the increase in ventilation that occurs in response to arterial hypoxemia Understand perfusion and ventilation and how it relates to each other, shunting • Ventilation: amount of air getting to the alveoli o Minute volume = RR x TV – normal is 6L/min o Alveolarventilation: how much air is getting to parts where gas exchange takes place – normal is 4.2L min – accounts for dead space (150 mL) § ABG – PaCO2 • Perfusion: amount of blood being sent to the lungs • Normal V/Qratio = 4L/min ventilation and 5L/min perfusion – 4/5 = 0.8 o Perfusion exceeds ventilation in the bases of the lungs because of gravity – lower ratio § Low PaO2 and high PaCO2 o Ventilation exceeds perfusion in the apices of the lungs – higherratio § High PaO2 and low PaCO2 o Changes will change normal ratio – can be physiologically controlled § Just by standing up! - V/Qmismatch • Shunting – steps taken to normalize the ratio, control perfusion, increase efficiency o Hypoxic(pulmonary artery) vasoconstriction § V/Qratio is low (too little ventilation or too much blood) § Causes blood coming into the area to be directed to other parts of the lung § Decreases the perfusion of the hypoxic region will raise the V/Q ratio and bring the arterial blood gases closer to what we expect § Most important cause: low alveolar partial pressure of oxygen (PaO2); also caused by acidemia and inflammatory mediators o Bronchoconstriction § V/Qratio is high (too much ventilation or not enough blood) § Causes bronchi to constrict slightly to increase the resistance and decrease the amount of ventilation coming into an area that is not well perfused § Limits the amount of alveolardead space that occurs and minimizes the ‘wasted work’ How is oxygen and carbon dioxide most commonly found in the body • Oxygen delivery o Ventilation of the lungs o Diffusion of oxygen from the alveoli into the capillary blood o Perfusion of systemic capillaries with oxygenated blood o Diffusion of oxygen from systemiccapillaries into cells • Carbon dioxide removal o Diffusion of carbon dioxide from the cells into systemic capillaries o Perfusion of the pulmonary capillary bed by venous blood o Diffusion of carbon dioxide into the alveoli o Removalof carbon dioxide from the lung by ventilation o Carbon dioxide transport § Amount of CO2 in blood is a significant factor in acid-base balance § Retainingtoo much CO2 will cause an increase in respiratory rate § 3 ways: dissolved in plasma, bicarbonate, carb-amino compounds • Bicarbonate: as CO2 moves into the blood is diffuses intothe RBC’s - carbonic anhydratse combines CO2 and H2O to form carbonic acid – carbonic acid dissocaites into HCO3 and H+ - H+ binds to hgb and the HCO3 moves out of the RBC into the plasma • 60% venous CO2 is in bicarbonate form • 90% arterial CO2 is in bicarbonate form • Alveolar oxygen o Oxygen absorbed from alveoli to blood – alveolar oxygen determined by rate of absorption into blood and rate of entry of new oxygen o Partial pressure normally 104 mmHg • Alveolarcarbon dioxide o Removed from alveoli o Partial pressure normally 40 mmHg; increases directly in proportion to rate of CO2 excretion; decreases in inverse proportion to alveolar ventilation • Principles of gas exchange o Diffusion in response to concentration gradients – pressure proportional to concentration § CO2 20 times as soluble as O2 o Diffusion depends on partial pressure of gas o Haldane Effect: Oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin which increases the removal of carbon dioxide Understand basicconcepts of the oxyhemoglobin curve and what it represents • Oxyhemoglobin association and dissociation o Hemoglobin molecules bind with oxygen – oxyhemoglobin § Binds in areas of high partial pressure and released in areas of low partial pressure § Continues to bind until hgb binding sites are saturated § Diffusion across alveolocapillary membrane – partial pressure of oxygen molecules is much greater in alveolar gas than it is in capillaries – promotes rapid diffusion from the alveolus into the capillary § Determinants of arterial oxygenation: rate of oxygen transport to the tissues in blood and rate at which oxygen is used by the tissues o When hemoglobin saturation and desaturation are plotted one graph, the result is a distinctive S-shaped curve known as the oxyhemoglobin dissociation curve • Oxyhemoglobin shift o Shift to the left/up § Hemoglobin's increased affinity for oxygen – promotes association in the lungs and inhibits dissociation in the tissues § Alkalosis (high pH) and hypocapniaand hypothermia o Shift to the right/down § Hemoglobin's decreased affinity for oxygen – increase in the ease with which oxyhemoglobin dissociates and oxygen moves into the cells § Happens when cells need more O2 § Acidosis (low pH) and hypercapniaand hyperthermia o Bohr effect: shift in the oxyhemoglobin dissociation curve caused by changes in CO2 and H+ concentration in the blood Understand and be able to identify and define abnormalbreathing patterns • Kussmaulrespirations (hyperpnea) o Slightly increased ventilatory rate, very large tidal volume, no expiratory pause • Cheyne-Stokes respirations o Alternating periods of deep and shallow breathing; apnea lasting 15-60 seconds, followed by ventilations that increase in volume until a peak is reached, afterwhich ventilation decreases again to apnea o Occurs with decreased brainstem blood flow • Hypoventilation o Alveolarventilation is inadequate in relationship to the metabolic demands o Leads to respiratory acidosis from hypercapnia(CO2 >44) o Causes: airway obstruction, chest wall restriction, altered neurologiccontrol of breathing • Hyperventilation o Alveolar ventilation exceeds the metabolic demands o Leads to respiratory alkalosis from hypocapnia(CO2 <36) o Causes: anxiety, panic attacks, head injury, severe hypoxemia Know how to identify and define hypercapnia, hypocapnia, hypoxia, and hypoxemia • Hypercapnia o Increased CO2 in the arterial blood (PaCO2>44) o Occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation/hypoventilation - retain too much CO2 – respiratory acidosis o Ex: drugs, brainstem (medulla) injury, spinal cord injury, NMJ dysfunction, respiratory muscle disfunction (myasthenia gravis), thoracic cage abnormalities, airway obstruction, sleep apnea • Hypocapnia o Decreased CO2in the arterial blood (PaCO2<36) o Caused by hyperventilation – blowing off too much CO2 – respiratory alkalosis o See hyperventilation above • Hypoxemia o Hypoxemia is decreased PaO2 in blood; hypoxia is decreased O2 in cells/reduced levelof tissue oxygenation o Most common cause: ventilation-perfusion abnormalities o Hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years o Inspired irritants increase mucous production, size and number of mucus glands, and bronchial edema – thick mucus compromisedlungs defenses o Hypertrophied bronchialsmooth muscle o Hypoxemia (V/Q mismatch) and hypercapnia o Airways collapse early in expiration – gas trapped in lungs o S/Sx: decreased exercise tolerance, wheezing and SOB, copious productive cough, polycythemia from chronic hypoxemia, decreased FEV1, increased infections o Acute bronchitis: acute infection or inflammation of airways or bronchi commonly following viral illness § Symptoms similar to pneumonia but no consolidation or chest infiltrates – nonproductive cough occurs in paroxysms and is aggravated by cold, dry, or dusty air • Emphysema o Permanent enlargement of the gas-exchangeairways accompanied by the destruction of the alveolar walls without obvious fibrosis o Loss of elastic recoil o Destruction of the alveoli occurs through the breakdown of elastin in the septa as s result of an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of the lung’s structural cells – also produces large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs) o Types: § Centriacinar (centrilobular): septaldestruction occurs in the respiratory bronchioles and alveolar ducts; upper lobes • Alveolarsac remains intact • Tends to occur in smokerswith chronic bronchitis § Panacinar (panlobular): involves the entire acinus; damage is more randomly distributed; involves lower lobes o Primary: inherited deficiency of the enzyme a1-antitrypsin o Secondary: caused by cigarette smoke, air pollution, occupational exposures, and childhood respiratory infections o S/Sx: dyspnea on exertion, at restwhen progressed, little coughing with little sputum, thin, tachypnea, prolonged expiration, use of accessory muscles, pursedlips, increased AP diameter, tripod positioning • COPD o Airflow limitation that is not fully reversible; usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases o Chronic bronchitis + emphysema o Risk factors: tobacco smoke, occupational dusts and chemicals, indoor and outdoorair pollution, any factor that affects lung growth during gestation and childhood, alpha1 antitrypsin gene mutation • Pulmonary HTN o Mean pulmonary artery pressure above 25 mmHg at rest o Causes: elevated left ventricular pressure, increased blood flow through the pulmonary circulation, obliteration or obstruction of the vascular bed, active constriction of the vascular bed produced by hypoxemia or acidosis o Patho: overproduction of vasoconstrictors (thromboxane) and decreased production of vasodilators (NO and prostacyclin); remodeling of pulmonary artery intima; resistance to pulmonary artery blood flow increasing the pressure in the pulmonary arteries; workload of the right ventricle increases and subsequent right ventricular hypertrophy – may be followed by failure and eventually death o S/Sx: masked by primary pulmonary or CV disease; chest x-ray shows enlarged pulmonary arteries and right heart border – echo shows right ventricular hypertrophy o Cor pulmonale – secondary to PAH – pulmonary HTN creating chronic pressure overload in right ventricle § S/Sx: heart appears normal at rest; decreased cardiacoutput and chest pain with exercise • Bronchogenic cancers o Most frequent cause of cancer death in the US; most common cause: cigarette smoking o Laryngeal § Risk factors: smoking, heightened with smoking and alcohol consumption, GERD, HPV § S/Sx: progressive hoarseness, dyspnea, cough o NSCLC § 85% of all lung cancers § Squamous cell carcinoma: nonproductive cough or hemoptysis § Adenocarcinoma: tumorarising from glands – asymptomatic or pleuritic chest pain and SOB § Large cell carcinoma: chest wall pain, pleural effusion, cough, sputum, hemoptysis, airway obstruction resulting in pneumonia o SCLC – neuroendocrine § 10-15% of all lung cancers § Worst prognosis – rapid growth and early metastasis § Strongest correlation with smoking § Arise from neuroendocrine tissue – ectopichormone secretion – paraneoplasticsyndromes • Hyponatremia (ADH); Cushing syndrome (ACTH); hypocalcemia (calcitonin); gynecomastia (gonadotropins); carcinoid syndrome (serotonin) o Lung carcinoid tumor § 5% of all lung cancers § Grow slowly and rarely spread • Atelectasis o Collapse of lung tissues § Absorption: gradual absorption of air from obstructed or hypo-ventilated alveoli § Compression: external compression on the lung § Surfactant impairment: decreased production or inactivation of surfactant o S/Sx: dyspnea, cough, fever, leukocytosis (inflammatory process) • Pulmonary edema o Excess waterin the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability – increased capillary hydrostaticpressure leads to fluid leaking into lung o Most common cause: left sided heart failure o Post-obstructive pulmonary edema: negative pressure pulmonary edema § Rare, life-threatening complication that can occur afterrelief of upperairway obstruction – obstruction causes negative pressure to build and build as breathing attempts occur § S/Sx: dyspnea, orthopnea, hypoxemia, increased WOB, pink frothy sputum • ARDS o Characterized by acute lung inflammation and diffuse alveolocapillary injury – injury to pulmonary capillary endothelium, increased capillary permeability, inflammation, surfactant inactivation, edema, atelectasis o Dyspnea and hypoxemia with poor response to oxygen supplementation – hyperventilation and respiratory alkalosis – decreased tissue perfusion, metabolicacidosis, organ dysfunction – increased WOB, decreased TV, and hypoventilation – hypercapnia, respiratory acidosis, worsening hypoxia – decreased cardiac output, hypotension, death • Pulmonary embolism o Occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble o Virchow triad: venous stasis, hypercoagulability, and injuries to the endothelialcells that line the vessels o Results in widespread hypoxic vasoconstriction, decreased surfactant, releaseof neurohumoral substances, atelectasis of affected lung segments further contributing to hypoxemia, pulmonary edema, pulmonary HTN, shock, and even death o S/Sx: sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, unexplained anxiety • Pneumothorax – see above Not on study guide: TB, abscess, pneumonia, CF, bronchiectasis, bronchiolitis Cardiac Understand the basics of cardiac muscle contraction • Restingmembrane potential is similar to skeletalmuscle (-85 to –95mV) - threshold potential is +105 • Caused by opening of fast sodium channels and slow sodium channels • Slow sodium channels are sodium-calcium channels – open slower and remain open for longer – allows for influx of large quantity of calcium and sodium ions to the interior of the cardiac muscle fiber – maintains prolonged period of depolarization causing the plateau in the AP – calcium ions enterduring plateau phase activating the contractile process • Cardiac muscle has low permeability to potassium afteronset of AP (not like skeletal) o Decreases the outflux of potassium; prevents early return of AP to resting value Understand volumes, EF, Cardiacoutput, preload, and afterload • Cardiac output: volume of blood flowing through eitherthe systemic or the pulmonary circuit o HR x SV = CO in L/min o Normal at rest is 5 L/mi o Factors that affect cardiac output: preload, afterload, Frank Starling Law, Laplace’s Law, heart rate, myocardial contractility § Preload: “filling pressure” • The pressure generated at the end of diastole (ventricular relaxation) o Represents fluid returning to the heart o Increased preload represents increased myocardialoxygen consumption – heart is working harder • Determined by: amounts of venous return to the ventricle, blood left in the ventricle after systole (end-systolic volume) • Right ventricle preload = CVP • Left ventricle preload = pulmonary artery occlusion or wedge pressure • When preload exceeds physiologicrange - furthermuscle stretching - decreased CO § Afterload: “resistance” • The resistance to ejection during systole o Increased afterload = increased work of the heart and oxygen demand o Caused by: vasoconstriction, valvular stenosis, increased blood volume • Decreased afterload: heart contracts more rapidly • Increased afterload: slows contractions and increases heart workload • Right ventricle afterload = PVR(pulmonary vascular resistance) • Left ventricle afterload = SVR (systemicvascular resistance) § Frank Starling Law: • Related to the volume of blood at the end of diastole/preload and stretch placed on the ventricle • Myocardial stretch determines the force of myocardial contraction • More stretch = increased force of contraction o Greaterstretch during diastole = greaterforce of contraction = greateramount of blood pumped out § Laplace Law: • Contractile force within a chamberdepends on the radius of the chamberand the thickness of its wall • Smallerchambers and thicker chamber walls equal increasedcontraction force o In ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force § Heart rate • Effected by cardiovascular control center (sympatheticand parasympathetic), neural reflexes (sinus arrythmia with inspiration and expiration; baroreceptor reflex; Bainbridge reflex [IV infusions]; and atrial receptors), and hormones and biochemicals (epinephrine, norepinephrine, thyroid hormone, growth hormone) § Myocardial contractility • Stroke volume: volume of blood ejected during systole (ventricular contraction) • Force determined by: stretch/preload, nervous system input (symp v parasymp), adequacy of myocardial oxygen supply • Positive inotropes: increase force of contraction o Norepinephrine (sympathetic), epinephrine (adrenalmedulla), thyroid hormone, dopamine • Negative inotropes: decrease force of contraction o Acetylcholine (vagus nerve) • Hypoxia decreased contractility • EF: amounts of blood ejected perheartbeat by the ventricles o SV/end-diastolic volume o Normal is 55% or higher o Indicator of ventricular function • Cardiac index: CI = CO/BSA - normal is 2.5-4 L/min/m2 • Decreased CO/CI - anything that causes decreased contractility or decreased blood flow to the heart o MI, shock, bradycardia, decreased SV, negative inotropes, increased vascular resistance, cardiac tamponade, hypovolemia, valvular heart disease, high PEEP • Increased CO/CI - anything that causes increased contractility or increased blood flow to the heart o HTN, decreased vascular resistance, pulmonary edema, increased metabolicstate, positive inotropes • Factors that regulate blood flow: degree of cardiac contractility, heart rate, venous return to the heart o Blood volume, patency of venous system, degree of arteriolar dilation, differential pressure, skeletal muscle pump, respiratory pump (inspiration causes increase in negative pressure that draws blood into the heart and increases venous return), velocity, viscosity, vascular compliance (opposite of stiffness – veins are more compliant) o Laminar versus turbulent flow o Poiseuille’s Law § Greaterthe resistance, the lowerthe blood flow Know different valves and which type they are • Ensure one way blood flow • AV valves: atrioventricular valves o Tricuspid: between right atrium and right ventricle; three leaflets or cusps o Bicuspid (mitral): between left atrium and left ventricle; two leaflets or cusps • Semilunarvalves o Pulmonic semilunarvalve: from right ventricle to pulmonary artery o Aortic semilunar valve: from left ventricle to the aorta • During atrial contraction: tricuspid and bicuspid (mitral) valves are open as blood is pushed from the atria to ventricles • During ventricular contraction: aortic and pulmonic valves are open as blood is pushed from ventricles to pulmonary system/systemic circulation Potassium and calcium do what to the heart • Excess K+ decreased contractility o Causes heart to become dilated and flaccid; slows heart rate o Hyperpolarization occurs – cannotinitiate AP • Excess Ca++ causes spastic contraction • Low Ca++ causes cardiac dilation o Calcium abnormalities are not as big of a concern – blood levels are more regulated Understand electricalpathway of the heart – basics. Know different nodes and what they do • SA node – internodalpathway – AV node – AV bundles – left and right bundles of Purkinje fibers • Begins in SA node (pacemaker of the heart) o Located in right atrium near entry of SVC o Spontaneously depolarizes from 60-100 BPM o Impulse spreads rapidly from SA node along individual atrial muscle cells to depolarize the right and left atria – causes atrial contraction • AV node (40-60 BPM) o Located in posteriorwall of right atrium immediately behind the tricuspid valve o Delays cardiac impulse – allows atria to empty blood into the ventricles before ventricularcontraction • AV bundles o Normally one-way conduction through bundles – prevents re-entry of conduction o The only conducting path between the atria and ventricles o Divides into left and right bundles o Transmission time between AV bundles and last of ventricular fibers is the QRS time (0.06 sec) • Purkinje fibers (20-40 BPM) o From AV node through AV bundle into ventricles o Fast conduction – large fibers transmit AP’s quickly – gap junctions enhance velocity § Similar to saltatory conduction Know sympathetic and parasympathetic effects on the heart • Sympathetic- “fight or flight” o Increases electrical conductivity and the strength of the myocardial contraction o Increased sinus node discharge, rate of conduction impulse TRUE (TOP TWO) • Secondary hypertension o Caused by altered hemodynamics from an underlying primary disease or drugs § Raises peripheral vascular resistance and/orcardiac output § Ex: renal artery stenosis, renalparenchymaldisease, pheochromocytosis • Complicated o Hypertrophy and hyperplasia with associated fibrosis called vascular remodeling – damages vessels • Malignant o Rapidly progressive HTN – diastolic usually >140 mmHg o Increased hydrostaticpressure cause fluids to leak – can lead to encephalopathy • Orthostatic o Decrease in systolic by 20 mmHgand diastolic by 10 mmHg with standing o Lack of normal BP compensation in response to gravitational changes on the circulation – leads to pooling and vasodilation o Acute (delay) versus chronic (secondary to disease) versus idopathic o S/Sx: fainting upon standing – may include impotence, boweland bladderdysfunction • S/Sx of HTN o Early: no othersymptoms besides elevated BP – silent disease o Sustained, uncontrolled leads to target organ damage § Heart disease, renalinsufficiency, CNS dysfunction, impaired vision, impaired mobility, vascular occlusion, edema Aneurysm patho • Local dilation or outpuching of a vesselwall or cardiac chamber • True aneurysms o Involvement of all three layers of the arterial wall o Fusiform cicumferential (entire circumference) or fusiform saccular (one outpouching sac) • False aneurysms o Leak between avascular graft and a natrural artery – extravascularhematoma/clot o Dissecting, sacular have tearthat form an outpouching sac – only outerlayer stretches • S/Sx: o Heart: dysrhythmias, heart failure, embolisms o Aorta: asymptomaticuntil it ruptures – then becomes painful o Thoracic: dysphagia, dyspnea are caused by pressure o Abdomen: flow to an extremity is impaired causing ischemia o • Complication: o Aortic dissection: tear in intima or aorta into which blood flows furtheringthe tear o Disrupts flow through arterial branches o Surgical emergency o S/Sx: ripping chest and pack pain, loss of pulses, BP’s different on arms; c-x-ray: wide mediastinum o Connective tissue disease are predisposing factors DVT patho • Clot in a large vein causing obstruction of venous flow leading to increased venous pressure • Risk factors: Virchow's triad – venous stasis, venous endothelialdamage, hypercoagulable state • May cause post-thromboticsyndrome – chronicpersistent pain, edema, alteration in limb function Atherosclerosis patho • Form of arteriosclerosis – thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall – plaque development o Leading cause of CAD and CV disease • Progression of disease o Endothelium injury – inflammation of endothelium – cytokines released – cellular proliferation – macrophage migration – LDL oxidation(foam cell formation) w/ oxidative stress – fatty streak – fibrous plaque – complicated plaque (ruptured plaque) Raynaud’s patho • Episodic vasospasm (ischemia) in the arteries and arterioles of the fingers • S/Sx: changes in skin color and sensation caused by ischemia FALSE (BOTTOM TWO) • Phenomenon: secondary to other systemic diseases or conditions • Disease: primary vasospasticdisorder or unknown origin o Attacks triggered by brief exposure to cold or emotionalstress • Tends to affect young women CAD pathogenesis and s/s • Patho o Any vascular disorderthat narrows or occludes the coronary arteries o Results in an imbalance between coronary supply of blood and myocardial demand foroxygen and nutrients o Most common cause: atherosclerosis o Non-modifiable risk factors: family hx, advanced age, male gender or women aftermenopause o Modifiable risk factors: dyslipidemia, HTN (endothelial injury, increased in myocardial demand), cigarette smoking (vasoconstriction and increase in LDL, decrease in HDL), DM and insulin resistance (endothelial damage, thickening of vessel wall), obesity and/or sedentary lifestyle o Non-traditionalrisk factors: § Markers of inflammation and thrombosis: CRP – released by liver; indirect measure of plaques and any inflammation § Troponin I § Hyperhomocysteinemia: result of geneticlack of enzymes that breaks down homocysteine (amino acid) or folate, b12, or b6 deficiency § Adipokines: group of hormones released from adipose cells – decreased = increased risk § Infection: inflammation of vessels – vascular disease § Air pollution § Coronary artery calcification, carotid wall thickness o Dyslipidemia: indicator of coronary risk § Increased LDL: role in endothelialinjury, inflammation, immune response that are important in atherogenesis § Low HDL: responsible for reverse cholesteroltransport – return excess cholesterolfrom tissues to liver § Elevated serum VLDL (triglycerides) § Increased lipoprotein a Angina pathogenesis and s/s • Unstable angina: reversible myocardial ischemia and a harbinger of impending infarction o Transient episodes of thromboticvesselocclusion and vasoconstriction occur at the site of plaque damage with a return of perfusion before significant myocardialnecrosis occurs • Stable angina: predictable chest pain with exertion • Prinzmetalangina (variant): unpredictable chest pain • Silent ischemia: no detectible symptoms; common with DM • Angina pectoris: transient substernalchest discomfort MI pathogenesis and s/s • Prolonged ischemiacauses irreversible damage to the heart muscle (myocyte necrosis) • Structural and functional changes: o Myocardial stunning: temporary loss of contractile function that persists for hours to days after perfusion has been restored o Hibernating myocardium: tissue that is persistently ischemicundergoes metabolicadaptation to prolong myocyte survival o Most common cause: acute rheumatic fever § Higher risk for developing afib and thrombi o Untreated leads to pulmonary HTN, edemaand right ventricular failure • Tricuspid stenosis o Same as mitral stenosis except occurs on right side of heart • Aortic regurgitation o Inability of the aortic valve to close properlyduring diastole o Murmur: diastolic murmur § Betweens2 and s1 o S/Sx: widened pulse pressure as a result of increased stroke volume and diastolic backflow o Cause: CT disorders, syphilis • Mitral regurgitation o Permits backflow of blood from the left ventricle into the left atrium – results in left ventricular hypertrophy because of increased volume in left atrium entering ventricle o Murmur: systolic murmur – presence of s3 (splashing sound) o Mostcommon cause: mitral valve prolapse and rheumaticheart disease • Tricuspid regurgitation o Leads to volumeoverload in the rightatrium and ventricle, increased systemic venous BP, and right heart failure – increases JVP/JVD o Murmur: systolicmurmurthat increases with inspiration • Mitral valve prolapse o Anterior and posteriorcusps of the mitral valve billowupward (prolapse) into the atrium during systole o Can cause mitral valve regurgitation; affected valves at greaterrisk for infective endocarditis § Genetic (x-linked) and environmental o S/Sx: asymptomatic • Pulmonicstenosis o Result of congenitalanomaly o Systolic murmur • Pulmonicregurgitation o Seen with pulmonary HTN – low pressure turned high pressure causing dilation of valve and regurg o Diastolic murmur Rheumatic fever and disease patho • Abnormalimmune response to the M proteins that cross react with normal tissues • Fibrinoid necrotic deposits: Aschoff bodies • S/Sx: o Carditis – murmur; polyarthritis – mainly large joints, chorea – sudden aimless irregular involuntary movements, erythema marginatum – truncal rash o Can cause valvular stenosis from inflammatory damage – most common cause of stenosis Right and left heart failure and what causes them • HF: the heart is unable to generate adequate cardiacoutput, resulting in an inadequate perfusion of tissues, or an increased diastolic filling pressure of the left ventricle, or both – inability of the heart to supply the metabolism with adequate circulatory volume and pressure o Risk factors: ischemicheart disease and HTN • Left heart failure o Systolic heart failure – ejection problem § Inability of the heart to generate adequate cardiac output to perfuse tissues Staging of Heart Failure Classes of Heart Failure § LVEF <40% - ventricular remodeling/hypertrophy § Manifestations are the result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation • S/Sx: dyspnea, orthopnea, cough with frothy sputum, fatigue, decreased urine output, edema, paroxysmal nocturnal dyspnea • PE: pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, S3 gallop (excess fluid slapping), evidence of underlying CAD or HTN o Diastolic heartfailure – filling problem § Pulmonary congestiondespite normal stroke volume and cardiac output or ejectionfraction § LVEF >40%; Heart failure with preserved ejection fraction § Decreased compliance of left ventricle and abnormal diastolic relaxation which leads to increased end diastolic pressure – transmitted to pulmonary circulation – causes pulmonary congestion § Causes: HTN, ischemia, afib, ventricular hypertrophy, aging, DM § S/Sx: non-specific; dyspnea, exercise intolerance, fatigue, weakness • Right heart failure o Seen with pulmonary disease = cor pulmonale o Normally due to left sided heart failure o Back up into the pulmonary system from left sided heart failure leads to eventual right heart failure § Other causes: intrinsic pulmonary disease, pulmonary HTN, COPD, volume overload conditions, infarcted right ventricle, congenital heart disease, PE, heart valve disease o S/Sx: pedaledema, ascites, hepatosplenomegaly, elevated JVP-JVD, sacraledema, nocturia, jaundice, coagulopathy Pediatric congenitalheart defects, identify different types, s/s and how they are classified • Heart failure • Acyanotic defects: allow shunting from high-pressure left heart to lower-pressure right heart; CHF sx – untreatedleads to pulmonary HTN o Patent ductus arteriosus (PDA) § Vessellocated between junction or main and left pulmonary arteries § Failure of ductus arteriosus to close results in persistent patency – allows blood to shunt from aorta to pulmonary artery causing left to right shunt § Results in increased pulmonary blood flow resulting in increased pulmonary venous return to the LA and LV with increased workload on the left side of the heart § S/Sx: dyspnea, fatigue, poor feeding; continuous, machinery-type murmur; risk for bacterial endocarditis o Atrial septal defect (ASD) § Abnormalopening between the atria – blood flows from high pressure left atria to low pressure right atria – leads to right atrial and ventricular enlargement § Major types: ostium primum defect (low in septum); ostium secundum (center – most common); sinus venosus (high in septum) § S/Sx: often asymptomatic; dx by murmur; pulmonary symptoms on exertion at later age o Ventricular septal defect § Abnormalcommunication between ventricles – shunting from high pressure left ventricle to low pressure right ventricle § Common congenitalheart lesion (25-33%); depends on size and degree of PVR • Pulmonary over-circulation accounts forsymptoms in large VSD § S/Sx: heart failure, poor weight gain, murmur and systolic thrill • Cyanotic defects: complex with right to left shuntingand cyanosis – obstruction causes increasedright sided pressure – still moves from high to low o Manifest with hypoxemia and cyanosis § Mild hypoxemia: occasional cyanosis § Severe hypoxemia: feeding intolerance, poor weight gain, tachypnea, dyspnea § Chronic hypoxemia: small for age, cognitive/motor delays, polycythemia, exertional dyspnea, easily fatigued, exercise intolerance, nail bed clubbing o Tetralogy of Fallot § Syndrome represented by four defects: • VSD; overriding aorta straddles the VSD; pulmonary valve stenosis; right ventricle hypertrophy § S/Sx: cyanosis and clubbing, feeding difficulty, squatting • Hypercyanoticspell or “tet spell” that generally occurs with crying and exertion RAAS system and humoral control of the CV system • Increases systemicarterial pressure and increases sodium reabsorption – increase BV/BP/RBF o Renin: enzyme formed and stored in afferent arterioles of JGA o Forms angiotensin I which is activated by ACE to angiotensin II o Angiotensin II § Stimulates secretion of aldosterone by the adrenal cortex § Is a potent vasoconstrictor § Stimulates ADH secretion Not on study guide: blood pressure control, dyslipidemia Acid/Base and Fluids Fluids • TBW: 42L; 60% weight o Intracellular fluid contains ⅔ TBW o Extracellular fluid contains ⅓ TBW o Two main fluids: § Interstitial fluid § Intravascular fluid – blood plasma § Ex: lymph, synovial, intestinal, CSF, sweat, urine, pleural, peritoneal, pericardial, intraocular • Osmosis: movement of water down concentration gradient • Osmolality: concentration of molecules per weight of water – controls osmosis • Osmotic forces: amount of hydrostatic pressure required to oppose or stop the osmotic movement of water o Determined by membrane thickness, size of molecules, concentration of molecule gradient, and solubility of molecules to the membrane Understand basics about capillary hydrostatic pressure, plasma oncotic/colloid pressure, interstitial pressure, and interstitial fluid oncotic/colloid pressure = Starling forces o Filtration: movement of fluid from the capillary into the interstitial space o Reabsorption: movement of fluid from the interstitial space into the capillary § FOUR FORCES determine whether there is reabsorption or filtration • Capillary hydrostaticpressure (BP) • Pushes water from the capillary to interstitial space • Capillary (plasma) oncotic pressure (from plasmaproteins in capillary) • Pulls waterfrom the interstitial space back into the capillary usingosmosis • Interstitial hydrostaticpressure • Pushes water from interstitial space into the capillary • Interstitial oncotic pressure (from plasmaproteins in interstitium) • Pulls waterfrom the capillary into the interstitial space using osmosis § Starling's Hypothesis: net filtration is equalto the forces favoring filtration minus the forces opposing filtration • Forces favoring filtration or forces opposing reabsorption: • Capillary hydrostaticpressure (BP) - push • Interstitial oncotic pressure - pull • Forces opposing filtration or forces favoring reabsorption: • Interstitial hydrostaticpressure - push • Capillary (plasma) oncotic pressure – pull § Majorforces for filtration and reabsorption are those within the capillary • Capillary hydrostaticpressure (BP) - push - filtration • Capillary (plasma) oncotic pressure - pull - reabsorption § Arterial end of the capillary • Hydrostatic pressure > interstitial oncotic pressure • Water pushes/filters into the interstitial space • Filtration § Venous end of the capillary • Capillary (plasma) oncotic pressure > intersitial hydrostaticpressure • Water is pulled into the circulation/capillary • Reabsorption § Integrity of capillary membraneis essential in capillary filtration of fluid Patho of edema • Edema: accumulation of fluid in the interstitial spaces o Causes: § Increased capillary hydrostatic pressure – ex: venous obstruction § Decreased plasmaoncotic pressure – ex: losses or diminished production of albumin § Increased capillary permeability – ex: inflammation and immune response – proteins leak § Lymph obstruction – ex: lymphedema § Sodium retention – increases hydrostatic pressure o Pathophysiology: § Increase in forces favoringfluid filtration from the capillaries or lymphatic channels into the tissues o Manifestations: § Localized: limited to site of trauma or specific organ system • Ex: sprained ankle; cerebral edema, pulmonary edema, ascites, plueraleffusion § Generalized • Ex: dependent edema § Associated with weight gain, swelling, tight clothes/shoes, limited ROM, and symptoms associated with underlying pathologic condition § Third-spacing • Fluid movement into space that is not available for metabolicprocesses or perfusion • Ex: interstitial space, pleural space, pericardial space Role of sodium in fluid balance • Sodium: most abundant ion in ECF – responsible forosmoticbalance of ECF – where Na is, waterfollows o Roles include: § Neuromuscularirritability, acid-base balance, cellular reactions, transport of substances o Normal: 135-145 mEq/L • Hormonal regulation of sodium o Aldosterone, natriureticpeptides, and natriuretic peptides and RASS Hormonal control of fluid; aldosterone, natriuretic peptides, and ADH basic functions • Water balance – also associated with Na balance o Aldosterone: a mineralocorticoid steroid synthesized and secreted from the adrenalcortex and acts on the distal tubule of the kidney § Secreted when blood sodium levels are depressed, potassium levels increase, orrenalperfusion is decreased § Leads to: § Hypernatremia • Water loss or sodium gain • Manifestations: o Convulsions, pulmonary edema, hypotension, tachycardia § Hyperchloremia • Causes: o Hypernatremia or bicarbonate deficit; secondary pathologic processes o No specificsymptoms § Water deficits • Dehydration, pure water deficits, renalfree water clearance • Manifestations: o Tachycardia, weak pulse, posturalhypotension, elevated hct, elevated serum sodium levels, headache, dry skin, dry mucous membranes • Isotonicsolutions: have same osmotic pressure across membrane o Free movement of water across the membrane without changing the concentration of solutes on either side o Osmolality between 275-300 o Isotonic alterations: § Total body waterchange with proportionalelectrolyte change – no change in concentration • Ex: hemorrhage, severe wound drainage, excess diaphoresis, intestinal losses, decreased fluid intake § Isotonicvolume depletion = hypovolemia § Isotonicvolume excess = hypervolemia Understand electrolyte abnormalities • Potassium: majorintracellular cation o Aldosterone, insulin, epinephrine, and alkalosis pull K into the cells o Aldosterone deficiency, insulin deficiency, strenuous exercise, and acidosis pull K out of the cells § Inverse relationship with H+ o Maintained by kidneys viaexcretion and by how much is assorted in the stomach from dietary sources as well as aldosterone and insulin secretion, and changes in pH o Purpose: § Essential for the transmission and conduction of nerve impulses, normalcardiac rhythms, and skeletal and smooth muscle contraction § Regulates ICF osmolality and deposits glycogen in liver and skeletalmuscle cells o Hypokalemia: <3.5 § Causes: • Reduced intake; increased entry into cell; increased loss; hyperaldosterone state; respiratory alkalosis (exchange with H+ to lower pH); diarrhea § Manifestations: • Membrane hyperpolarization causes – decreased neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, cardiac dysrhythmias, U wave on ECG o Hyperkalemia: >5.5 § Causes: • Increased intake; shift to ECF; decreased excretion; hypoaldosterone state; hypoxia; acidosis (exchange of H+ in to increase pH); insulin deficiency; cell trauma § Manifestations: • Mild: tingling, restlessness, intestinalcramping and diarrhea, peaked T waves on ECG; cells are more excitable • Calcium • Severe: muscle weakness, loss of muscle tone, flaccid, paralysis, cardiac arrest; with very severe the cells become unexcitable because they are near or exceeding the RMP o Bones and teeth, blood clotting, hormone secretion, cell receptor function, muscle contractions o Normal: 8.6-10.5 o Regulated by: § PTH: • Increases via kidney reabsorption • Secreted in response to low serum calcium § Vitamin D • Increases calcium absorption from GI tract; enhances renaland bone absorption § Calcitonin • Decreases plasmacalcium levels by inhibiting absorption in gut and kidney o Hypocalcemia: <8.5 § Causes: • Inadequate intake or absorption; decreases in PTH and vitamin D; blood transfusions § Manifestations: • Increases neuromuscularexcitability (partial depolarization) • Muscle spasms, convulsions, tetany • Chvostek (tap facial nerve – twitch) and Trousseau (BP cuff – wrist twitch) signs o Hypercalcemia: >12 § Causes: • Hyperparathyroidism – increased PTH; bone mets; excess vitamin D; immobilization; acidosis § Manifestations: • Decreased neuromuscular excitability • Muscle weakness, kidney stones, constipation, heart block • Hypophosphatemia o Causes: intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse o Manifestations: diminished release of oxygen, osteomalacia, muscle weakness, bleeding disorders, leukocyte alterations • Hyperphosphatemia o Causes: exogenous orendogenous addition of phosphate to ECF, long term use of phosphate enemas or laxatives, renal failure o High phosphate levels associated with low calcium levels o Manifestations: same as hypocalcemiawith possible calcification of soft tissue • Chloride o Extracellular ion; tends to follow sodium; inverse relationship to bicarbonate o Importantanion in maintenance of iron balance and in gastric juice • Magnesium: 1.8-2.4 o Intracellular cation; stored in muscle and bones; interacts with calcium; involved in neuro excitability o Hypomagnesemia § Causes: malabsorption, hypocalcemiaand hypokalemia § Manifestations: neuromuscular irritability, tetany, convulsions, increased reflexes o Hypermagnesemia § Causes: renal failure § Manifestations: skeletalmuscle depression, muscle weakness, hypotension, respiratory depression, bradycardia Understand how to classify and identify different acid/base imbalances – Metabolic/respiratory acidosis/alkalosis • pH: negative logarithm of the H+ concentration o H+ high: low pH – acidic o H+ low: high pH – alkaline o To maintain the body’s normal pH the H+ must be neutralized by the retentionof bicarbonate or the excretion of H+ § Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes § Regulated by bones, lungs, kidneys • Renal regulation (slow) or pulmonary regulation (fast) • Metabolicacid-base function or respiratory acid-base function o pH < 6.8 or > 7.8 = death • Acidosis: pH less than 7.35 o Systemicincrease in H+ or loss of base • Alkalosis: pH greaterthan 7.45 o Systemic decrease in H+ or excess of base • Respiratory acidosis o Elevation of pCO2 as a result of ventilation depression or alveolar hypoventilation; causes true hypercapnia § Causes: brainstem trauma, over sedation (depression of respiratory center), respiratory muscle paralysis, disorders of the chest wall, disorders of the lung parenchyma § Compensation: not as effective since kidneys are slow to conserve bicarb and eliminate H+ § Labs: pH <7.35; CO2>45 § Manifestations: headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma • Must be carefulwith correcting because rapid reduction of PCO2 can cause respiratory alkalosis with seizures and death • Respiratory alkalosis o Depression of pCO2 as a result of hyperventilation; causes hypocapnia § Causes: high altitudes, hypermetabolic states (fever, anemia, thyrotoxicosis), early salicylate intoxication, anxiety or panic disorder, improper use of ventilators § Compensation: kidneys decreases H+ excretion and absorb bicarbonate § Labs: pH >7.45; CO2 <38 § Manifestations: dizziness, confusion, paresthesia's, convulsions, coma, signs of hypocalcemia • pH increased – less acid to compete with calcium - calcium binds with free albumin – decreases serum calcium • Metabolicacidosis o Depression of HCO3- from ECF or an increase in noncarbonicacids § Causes: lactic acidosis, renal failure, DKA, starvation § H+ move to intracellular space and K+ moves to extracellular space to maintain ion balance (both +) § Compensation: respiratory hyperventilation – decreasing carbonicacid § Labs: pH <7.35; HCO3- <24 • Filtration: plasmafiltrate from glomerulus passes through the glomerularmembrane into the Bowman space to form the primary urine • Vasculature: o Supplied by the afferent arteriole and drained by efferent arteriole o JGA: site of regulation of renal blood flow, glomerular filtration, and renin secretion § JG cells located around afferent arteriole (store renin – detect blood flow or pressure and will secrete renin if needed to increase BV/BP) § Macula densa: portion of distal convoluted tubule with specialized sodium and chloride sensing cells; located between afferent and efferent arterioles; decreased Na/Cl will stimulate and cause vasodilation and increased hydrostatic pressure § Renal tubules • Proximal: lined with microvilli to increase surface areaand reabsorption • Loop of henle: transport solutes and water; contributes to hypertonicstate of renal medulla • Distal: adjusts acid-base balance by excreting acid into the urine and forming new bicarbonate ions • Collecting duct: resorb sodium and waterand excrete potassium and cells that secrete hydrogen or bicarbonate and potassium o Ureters § 30 cm long; smooth muscle; peristaltic activity § Micturition compresses the lowerend of the ureter to avoid urine reflux o Bladder § Detrusormuscle (smooth muscle); trigone (between opening of 2 ureters and urethra and detects stretch of bladder) o Urethra § Internalsphincters (smooth muscle under involuntary control) § Externalsphincter (skeletalmuscle under voluntary control) § 3-4 cm in women; 18-20 cm in men o Innervation of bladder and urethra § Parasympathetic fibers (autonomic) • Bladder, internal urethral sphincter • Contracts detrusor muscle § Sympathetic fibers (autonomic) • Allows bladderto fill § Skeletalmotor neurons in pudendal nerve (somatic) • Externalurethral sphincter – voluntary • Damage can cause incontinence • Micturition – urination GFR, importance, how regulated, what it represents • Glomerular Filtration Rate: filtration of plasma into the Bowmanspace per unit of time o Normal >60% o Directly related to the perfusion pressure in the glomerularcapillaries o If MAP decreases or vascular resistance increases – renal blood flow and GFR decreases • Regulation: o Autoregulation § 80-180 mmHg provides constant GFR • BP increases - afferent arterioles constrict to prevent increase in filtration pressure and vice versa • Prevents wide fluctuation in BP being transmitted to glomerularcapillaries § Myogenicmechanism (stretch) • Decrease in systemicpressure - glomerularperfusion increases o Stretch on afferent arteriolar smooth muscle decreases – arteriole dilates– more blood delivered to glomerulus • Increase in system pressure – glomerularperfusion decreases o Arteriole smooth muscle contracts – decreases blood flow to glomerulus § Tubuloglomerular feedback (NaCl content) • When sodium filtration increases - GFR decreases o Macula densacells sense and stimulate afferent arteriolarvasoconstriction • When sodium filtration decreases – GFR increases o Afferent arterioles vasodilate o Neural regulation § Sympathetic nervous system • Vasoconstriction – decreased GFR § Baroreceptor reflex • Vasoconstriction of afferent arterioles with activation of a1-adenoreceptors – decreases perfusion and GFR § Exercise and change of body position • Activate renal sympatheticneurons – causes mild vasoconstriction § Severe hypoxia • Stimulation of chemoreceptors; decreases renalblood flow by sympatheticstimulation o Hormones (RAAS) - review § Increases systemic arterial pressure and increases sodium reabsorption – increase BV/BP/RBF • Renin: enzyme formed and stored in afferent arterioles of JGA • Forms angiotensin I which is activated by ACE to angiotensin II • Angiotensin II o Stimulates secretion of aldosterone by the adrenal cortex o Is a potent vasoconstrictor o Stimulates ADH secretion and thirst sensation RAAS system basics – see above Concentration of urine • Via nephron – filtration, tubular reabsorption, tubular secretion, excretion • Glomerular filtration: o Freely permeable to waterand relatively impermeable to large colloids such as plasma proteins § Importantpermeability factors: size and electrical charge § + more permeable o Net filtration pressure = forces favoring (capillary hydrostaticpressure – push) and forces opposing (capillary oncotic pressure and hydrostatic pressure in Bowman capsule – pull) § Also glomerularhydrostatic pressure, capsular hydrostaticpressure, blood oncotic pressure • Concentration of urine o Begins in proximaltubule § Active reabsorption of majority of sodium o Concentration occurs in the Loop of Henle § Descending loop: water reabsorption, sodium diffuses in § Ascending loop: sodium reabsorbed by active transport, waterstays in § Ureasecretion in thin segment o Distal tubule § Reabsorption of sodium and wateronly with ADH, bicarbonate § Secretion of potassium, urea, hydrogen, drugs o Collecting ducts § Reabsorption of wateronly with ADH § Reabsorption of secretin of sodium, potassium, hydrogen § Final concentration of urine completed § Peds and renal function • Decreased ability to remove excess water and solutes; decreased concentrating ability • Narrow margin for fluid and electrolyte balance • Increased risk for dehydration • Increased risk for drug toxicity Aging and renal function • Decrease in renal blood flow and GFR o Altered sodium and water balance • Number of nephrons decrease due to renalvascular and perfusion changes • Response to acid-base changes is delayed • Increased risk for drug toxicity • Alterations in thirst sensation and waterintake leading to dehydration • S/Sx: o Hematuria (microscopic – early) o Dull and aching flank pain o Palpable flank mass in thinnerindividual o Systemic: present in advanced stage, weight loss, fatigue, tumor fever, anemia (hematuria and lack of EPO), HTN (elevated renin), altered liver fxn tests o Early stage is oftensilent o Mets: lung, lymph nodes, liver, bone, thyroid, CNS • Bladder tumors o Urothelial (transitionalcell) carcinoma mostcommon o Risk factors: males >60, smoking, exposure to metabolites of dyes, amines, or chemicals; arsenic in water, phenacetin consumption o Patho: § Oncogenes of ras gene and TP53 mutation of tumorsuppressorgenes § Papillary more common § Can develop as secondary cancer by invasion of othercancers from borderline organs o S/Sx: § Gross painless microscopic hematuria – often recurrent and associated with UTI symptoms § May have flank pain with tumor growth and obstruction § Cause of death is often mets UTIs, s/s, patho • UTI: inflammation of the urinary epithelium afterinvasion and colonization of pathogens in the urinary tract; retrograde movement of bacteria o Classification § Complicated (functional or anatomical dysfunction) vs. Uncomplicated § Cystitis: bladderinflammation (not UTI) § Pyelonephritis: inflammation of upperurinary tract • Patho o Protective mechanisms: washed out during urination, acidic and high osmolality of urea, Tamm-Hosfall protein (antimicrobial), bactericidal secretions, ureterovesicaljunction (closes to prevent reflux), mucus secreting glands in women, length of male urethra men, Lewis blood group more prone o Pathogens: E. coli and staphylococcus saprophyticus § Virulence: ability to evade, adherence to uroepithelium, resist host’s defensemechanism § Phagocytosis of bacteria in urine maximized at pH of 6.5-7.5 • S/Sx o Frequency, dysuria, urgency, low back or suprapubic pain • Cystitis: inflammation of bladder o Acute or chronic o Asymptomatic or s/sx of UTI without the presence of bacteria • Interstitial cystitis: nonbacterialinfectious cystitis o Result of autoimmune reaction responsible for inflammatory response that includes mast cell activation, altered epithelial permeability, and increased sensory nerve sensitivity o S/Sx: most common in women 20-30 years old and immunocompromised; bladderfullness, frequency, small urine volume, chronic pelvic pain, negative urine cx Pyelonephritis • Infection of one or both upper urinary tracts (ureter, renalpelvis, and interstitium) o Acute pyelonephritis: acute infection of the renal pelvis interstitium – *E. Coli, proteus, pseudomonas § Inflammatory process usually focal and irregular – affects pelvis, calyces and medulla § Causes medullary infiltration of SBC’s with renal inflammation, edema, and purulent urine § Affects tubules – glomeruli spared § 2 step process: bacteria attach and cause inflammatory response – release of mediators cause increased permeability and WBC’s are able to get into urine § S/Sx: • Acute onset of symptoms with fever, chills, and flank and groin pain; UTI s/sx • Older adults have non-specificsymptoms: low grade fever, malaise – need to catch – urosepsis o Chronic pyelonephritis: persistent or recurring episodes of acute that lead to scarring § Risk increases with renal infections and obstructive pathologic conditions – prevents elimination of bacteria – progressive inflammation – alteration of renalpelvis and calyces – destruction of tubules – atrophy, dilation, and diffuse scarring – impaired urine concentrating ability § S/Sx: • Early (mild; HTN, frequency, dysuria, flank pain); Loss of tubular function (inability to conserve sodium, hyperkalemia, metabolic acidosis); progressive (renal failure) Glomerulonephritis, patho, s/s, types • Patho o Formation of immune complexes in circulation – deposit in glomerulus o Antibodies produced against organism that cross-reactwith glomerular endothelialcells o Activation of complement system – recruitment and activation of immune cells and mediators o Decreased GFR – decreased glomerular perfusion from inflammation, glomerular sclerosis/scarring, thickening of the glomerular basement membrane, increased permeability to proteins and RBC’s • S/Sx: o Hematuria with RBC casts (smoky, brown-tinged urine), proteinuria (3-5g/day w/albumin) - low serum albumin and edema from lack of albumin, severe orprogressive glomerular disease – eventualoliguria § Oliguria: output<30 mL/hr or <400 mL/day • Types o Nephrotic sediment § Contains massive amounts of protein and lipids – microscopic or no blood o Nephritic sediment § Blood is present with RBC casts, WBC casts, varying degrees of protein (usually not severe) § Caused by increased permeability of the glomerularfiltration membrane due to systemic immune complexes or infection leading to inflammation o Chronic § Progressive course leading to chronic kidney failure § Reduction in nephron mass – compensatory hypertrophy and hyperfiltration – interglomerular HRN (to try to increase GFR in remaining healthy nephrons) - sclerosis and further nephron loss § S/Sx: proteinuria, hypercholesterolemia Nephrotic syndrome, s/s patho • Excretion of 3g or more of protein in urine as a result of glomerularinjury • S/Sx: o Foamy urine, hypoalbuminemia (peripheral edema), prone to infection (loss of immunoglobulin), vitamin D deficiency, hyperlipidemia/lipiduria (from liver compensating for lack of protein), hypothyroidism AKI patho • Sudden decline in kidney function with a decrease in GFR and accumulation of nitrogenous waste products in the blood o Uremia: urea in blood – syndrome of renal failure § Elevated BUN and creatinine; fatigue, anorexia, N/V, pruritis, neuro changes, retention of toxic wastes, electrolyte disorders, proinflammatory state § Manifestation of azotemia • Azotemia: increased serum urea levels and frequently increased creatinine levels • Caused by renal insufficiency or renal failure • Measured clinically but no symptoms • Increase in serum creatinine and BUN • Results from extracellular volume depletion, decreased renalblood flow, or toxic/inflammatory injury to the kidney cells • 3 categories: prerenal, intrarenal, postrenal Prerenal, intrarenal, postrenal • Prerenal: renal hypoperfusion o *Most common cause of ARF o Occurs rapidly overhours – is reversible o Elevation of BUN and creatinine, GFRdeclines because of decrease in filtration pressure • Intrarenal: involves the renal parenchymal or interstitial tissue – acute tubular necrosis caused by ischemia o Occurs most often aftersurgery; also - sepsis, obstetriccomplications, severe trauma, burns o Injury effectsmostly proximal tubules and thick ascending limp of loop of Henle – decreased GFRcaused by obstruction of lumens o Post ischemic or nephrotoxic