NR 507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXIT 2026. Comprehensive Study Guide.

NR 507: ADVANCED PATHOPHYSIOLOGY MIDTERM/EXIT 2025 [Document subtitle] [DATE] [COMPANY NAME] [Company address]Hypersensitivity: Type 1 Type 1: Allergic reaction, Mediated by IgE, Inflammation due to mast cell degranulation Local symptoms: -itching -rash Systemic symptoms: -wheezing Most dangerous = anaphylactic reaction systemic response of hypotension, severe bronchoconstriction Main treatment: epinephrine reverses the effects Hypersensitivity: Type 2 Type 2: Cytotoxic reaction; tissue specific (ex: thyroid tissue) Macrophages are the primary effectors cells involved Can cause tissue damage or alter function Grave's disease (hyperthyroidism) - example of altering thyroid function, but does not destroy thyroid tissue Incompatible blood type- example of cell/tissue damage that occurs; severe transfusion reaction occurs and the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis. Type 1 Hypersensitivity VS. Type 2 Hypersensitivity Type 1 Hypersensitivity Organ Specific Antibody binds to the antigen on the cell surface Type 2 Hypersensitivity Not Organ Specific Antibody binds to the soluble antigen outside the cell surface that was released into the blood or body fluids, and the complex is then deposited in the tissues Hypersensitivity: Type 3 - Examples Rheumatoid arthritis: Antigen/antibodies are deposited in the jointsSystemic Lupus Erythematosus (SLE)- very closely related to autoimmunityantigen/antibodies deposit in organs that cause tissue damage Hypersensitivity: Type 4 Delayed response Does not involve antigen/antibody complexes like Types 1, 2 and 3 Is T-cell mediated Differentiating Between the Rash of a Type 1 vs. Type 4 Reaction: Type 1: Immediate hypersensitivity reactions, termed atopic dermatitis, are usually characterized by widely distributed lesions Type 4: Contact dermatitis (delayed hypersensitivity) consists of lesions only at the site of contact with the allergen The key determinant is the timing of the rash: -Type 1 = Immediate -Type 4 = Delayed: Several days following contact, ex would be poison ivy Treatment of Type 4 Rash A non-severe case of contact dermatitis would be treated with topical corticosteroid. Why not epinephrine or antihistamines? -Epinephrine is for emergent Type 1 anaphylactic reactions. Antihistamines act on the H1 receptors. Type 4 does not involve mast cells and H1 receptors. Antibiotics not appropriate since not an infection Autoimmunity Autoimmune disease can be familial, Affected family members may not all develop the same disease, but several members may have different disorders characterized by a variety of hypersensitivity reactions, These include autoimmune and allergic reactions Associations with particular autoimmune diseases have been identified for a variety of major histocompatibility complex (MHC) alleles or non-MHC genes Alloimmunity General term used to describe when an individual's immune system reacts against antigens on the tissues of other members of the same species.Examples: Neonatal disease where the maternal immune system becomes sensitized against antigens expressed by the fetus, Transplant rejection, Transfusion reaction Primary Immunodeficiency Most primary immune deficiencies are result of single gene defects Something is lacking with the immune system itself. Example: B-lymphocyte deficiency - one of the most severe forms of a primary immunodeficiency Secondary Immunodeficiency Complication of some other physiological condition/disease, Malnutrition one of most common causes worldwide. Example: Pt. with HIV gets pneumocystis carinii Hematology Anemias, Involve RBCs, Most of body's iron stores come from the recycling of iron from old RBCs Iron Deficiency Anemia Microcytic/Hypochromic Anemia, Caused by disorders of hemoglobin synthesis, particularly iron deficiency, Ferritin is an important measurement that reflects the body's total iron stores, The NP will order a ferritin level to get an idea of the body's total iron stores, Low ferritin reflects anemia Major Lab Marker for Anemia Increased RBC distribution width (RDW) is one of the earliest lab markers in developing microcytic or macrocytic anemia Folate Deficiency Can cause megaloblastic anemia, Alcoholics can easily get folate deficiency Ferritin level normal Hgb low Hct low Vitamin B-12 Deficiency Fatigue, Dyspnea, Peripheral Neuropathy in BLE (numbness and tingling) Risk Factors: Older adults, H-pylori infection Affects Vitamin B-12 absorptionHemolytic Anemia Who is at risk? RBCs destroyed, Mismatched blood types destroy RBCs. Autoimmune hemolytic anemia due to autoantibodies against erythrocytes that the immune system perceives as an antigen and then attacks it. Allergic reaction to a drug causes drug-induced hemolytic anemia Acute Blood Loss Anemia Trauma victims who are losing blood, GI bleed (Acute) Aplastic Anemia Diagnosis made by blood tests and bone marrow biopsy. AA is suspected if levels of circulating erythrocytes, leukocytes and platelets diminished: -Granulocyte count less than 500/ uL -Platelet count less than 20,000/ uL -Absolute reticulocyte count less than or equal to 40 x 109/ L Sickle Cell Anemia Patients encountered who have sickle cell trait, Inherited a normal Hb gene from one parent and an abnormal Hb gene from the other parent Thalassemia Inherited blood disorder causing decreased circulating hemoglobin, Many possible genetic mutations Heart Failure Pathophysiology (Wk 2 Discussion) Underlying patho is that there is less cardiac output to meet the body's oxygen demands. Over time there is decreased contractility, decreased stroke volume, increased left ventricular end-diastolic volume (LVEDV) When contractility is decreased, stroke volume falls, and LVEDV increases. This causes dilation of the heart and an increase in preload. Major risk factor is long standing hypertension. Preload = stretch Afterload = resistance Differentiate between Right and Left Heart Failure Sometimes right-sided heart failure can occur due to left-sided heart failure due to the back up of fluid from the left side to the right.Sometimes right-sided heart failure can occur without there being left-sided heart failure; this usually occurs because the person has long standing pulmonary issues (COPD). Patients will have classic R. sided heart failure symptoms without L. sided heart failure symptoms: Right JVD distention, Peripheral edema, Hepatosplenomegaly Stages of Heart Failure (ACC/AHA) -Stage A: patient has risk factors (CAD) but no symptoms; no structural heart damage -Stage B: patient has structural heart damage (MI), but still has no symptoms -Stage C: patient is symptomatic with alteration in their daily functions due to dyspnea, swelling, etc. This is where the NYHA functional classifications come into play -Stage D: end-stage heart-failure - have maximized medications to treat it. May need heart transplant or pacemaker NYHA Functional Classifications- It's all about the impact on the patient's activity caused by the HF symptoms: -Stage I: Mild- no limitation of physical activity; Ordinary physical activity does not cause symptoms -Stage II: Mild- slight limitation of physical activity; comfortable at rest; Ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain. -Stage III: Moderate- marked decrease in physical activity; marked limitation of physical activity; comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain. -Stage IV: Severe- inability to carry on any physical activity without discomfort. Symptoms of HF or the anginal syndrome may be present even at rest. If any physical activity undertaken, discomfort is increased. Heart Valve Disorders Signs and Symptoms (Edapt Scenarios), Murmur Characteristics, Important to know Anatomy Aortic Stenosis Blood backed up into left ventricle causing perfusion problems for the rest of the body Causes: Bicuspid aortic valve- congenital condition (only two cusps to the aortic valve which usually has three cusps)- the two cusps get damaged quicker because they are doing the work of three Age related calcification- obstruction/ stenosis Smoking, High BP, Hypertension, Hyperlipid, Diabetes Rheumatic Fever Signs & Symptoms = SADS: Syncope A: Angina D: Dyspnea **Fainting Chest pressure upon exercising Sustained, laterally displaced apical pulse Mid-systolic crescendo-decrescendo murmur heard loudest at base and radiating to the neck S4 gallop present** Aortic Regurgitation Blood is coming back from the Aorta into the L. Ventricle through the Aortic Valve Causes Widening or aneurysmal change of the aortic annulus (ring of fibrous tissue surrounding the aorta) Endocarditis Rheumatic Fever Signs & Symptoms Fatigue Syncope SOB Palpitations Widened Pulse Pressure L. Ventricular Dilation Early diastolic murmur along left sternal border **Shortness of breath that progressively worsens High pitched early diastolic murmur heard loudest at left lower sternal border Diastolic rumbling sound at the heart's apex Systolic crescendo-decrescendo murmur heard at the left upper sternal border A chest x-ray may show signs of pulmonary edema and cardiomegaly** Mitral Stenosis Blood is going to back up into the L. Atrium and Lungs Causes Rheumatic Fever / Rheumatic Heart Disease EndocarditisSigns & Symptoms Fatigue SOB Exercise intolerance Cough L. Atrial enlargement Pulmonary congestion/edema Diastolic rumble Opening snap before Diastolic rumble **As mitral stenosis progresses, symptoms of decreased CO occur, especially during exertion Shortness of breath on activity Pounding/racing heart Associated w/ history of Rheumatic HD A low-pitched murmur auscultated at the heart's apex JVD and bilateral crackles in lung bases noted ECG demonstrates A-FIB and Left Ventricular Hypertrophy** Mitral Regurgitation Blood goes from L. Ventricle to L. Atrium and then to the Lungs Causes - Anything that causes LV dilation Remodeling process (post MI) Dilated cardiomyopthathy Rheumatic Fever/ Rheumatic Heart Disease Endocarditis Papillary muscle dysfunction/rupture/ chordae tendinae Calcification of the valve/around the valve Signs & Symptoms Acute Chronic **Shortness of breath JVD, Crackles in bilateral lung bases Blowing pansystolic murmur heard best at heart's apex and radiates to back and axilla** Obstructive vs. Restrictive Pulmonary Disease Obstructive: decreased FEV1 indicates airway obstruction along with low FEV1/FEV ratio 56%Restrictive: FEV1/FVC ratio above 70%, Review EDapt examples Asthma Airways constricted Intrinsic: triggered by something internal such as anxiety Extrinsic: triggered by something in outside environment- something in the air (dust mites/pet dander) In mildest form of asthma (intermittent), short acting beta2-agonist inhalers are prescribed Mild-persistent asthma will have night symptoms 3-4 days a month COPD Diagnosis based on Hx of symptoms, physical exam, chest imaging, pulmonary function tests and blood gas analysis Pulmonary function testing reveals airway obstruction (decreased FEV1) that is progressive and unresponsive to bronchodilators, Emphysema, Chronic bronchitis COPD Staging According to GOLD Guidelines- Based on degree of airway limitation Gold 1: Mild: FEV1≥80% predicted Gold 2: Moderate: 50% ≤FEV1 80% predicted Gold 3: Severe: 30% ≤FEV1 50% predicted Gold 4: Very Severe: FEV 30% predicted Emphysema Damage occurs in the alveoli, Impairs gas exchange, Issue is in expiration- they can get air in but cannot get air out Air trapping, Pursed lip-breathing Increased A&P diameter, Barrel chest Chronic Bronchitis Productive cough with copious amounts of sputum dyspnea wheezing rhonchi and cyanosis of the skin and mucous membranes Damage occurs in the airway- not the alveoli, Mucous Plugs Forced Vital Capacity (FVC)Normal 80-120% The FVC measures the volume of air in the lungs that can be exhaled. Patient inhales as deep as possible and then exhales as long and as forcefully as possible. Obstructive: Will be decreased or normal Restrictive: Will be decreased Forced Expiratory Volume in 1 second (FEV1) Normal 80-120% Amount of air forcefully exhaled from the lungs in the first second. The patient inhales and forcefully exhales as fast as possible. Obstructive: Will be decreased Restrictive: Will be decreased FEV1/FVC ratio Determines if the pattern is obstructive, restrictive or normal Normal is 70% or less than the lower limit of normal for the patient This is a calculated ratio that represents the proportion of a person's vital capacity that they are able to expire in the first second of forced expiration to the full, forced vital capacity. Obstructive: Less than 70% Restrictive: Normal or 70% Diffusing capacity The diffusing capacity is simply how well the lungs are able to exchange gas Residual volume (RV) RV is the amount of air that remains in the lungs after a forceful exhalation Total Lung Capacity (TLC) RV + FVC = TLCNormal range is 80-120% of predicted Obstructive: 120% (represents hyperinflation) Restrictive: 80% Microcytic anemia (MCV80 fL) describes RBCs that are small. Iron deficiency Sideroblastic Thalassemia Anemia of chronic disease Macrocytic anemia (MCV100 fL) describes RBCs that are large. B12 deficiency (pernicious anemia) Folate deficiency Normocytic anemia (MCV 80-99 fL) describes RBCs that are normal in size. Anemia of inflammation and chronic disease Hereditary spherocytosis G6PD deficiency Paroxysmal nocturnal hemoglobinuria Hypochromic anemia RBCs with less hemoglobin than normal. As a result, the RBCs appear pale in color (MCHC is low). Hyperchromic anemia RBCs with more hemoglobin than normal. As a result, the RBCs appear a dark hue or red than normal cells (MCHC is high). Normochromic anemia RBCs that have a normal amount of hemoglobin. As a result, the RBCs appear neither pale nor dark (MCHC is normal). Decreased tissue oxygenation from anemia can manifest as signs and symptoms of the following:Severe fatigue Pallor Weakness Dyspnea Dizziness Cardiac Output (CO) The amount of blood that the heart pumps in 1 minute. CO is also known as cardiac contractility. CO=heart rate (HR) x stroke volume (SV). Stroke Volume (SV) The volume of blood pumped out of the left ventricle during each systolic cardiac contraction. Afterload The force, or load, which the heart must contract against in order to pump blood. Afterload is also known as systemic vascular resistance (SVR). Preload The amount of stretch that the cardiac muscle exhibits at the end of ventricular filling. Right-sided Heart Failure S/Sx: Jugular vein distention Hepatosplenomegaly Peripheral edema CorPulmonale Tricuspid valve damage Right ventricle superior vena cava (preload) pulmonary artery (afterload) Causes of right heart failure include: 1) pulmonary disease that causes pulmonary hypertension. This is the most common cause; 2) right ventricular myocardial infarction (MI), which weakens the cardiac muscle; 3) right ventricular hypertrophy (secondary to cardiac damage); 4) tricuspid valve damage (causing backflow of the blood into the rightatrium or right ventricle after ejection); 5) secondary failure as a result of left heart failure due to the build-up of pressure in the damage left ventricle Left-Sided Heart Failure S/Sx: Increased left ventricular afterload Decreased ejection fraction Increased left ventricular preload Pulmonary edema Dyspnea Left ventricle Pulmonary vein (preload) Aorta (afterload) This increased pressure will force fluid from the pulmonary capillaries into the pulmonary tissues, which essentially floods those areas. The result is pulmonary edema and dyspnea. If left ventricular heart failure is unresolved, volume and pressure will continue to build until it reaches the right side of the heart, contributing to right heart failure as well Asthma Chronic disease due to bronchoconstriction and an excessive inflammatory response in the bronchioles What are 5 s/s of asthma coughing wheezing shortness of breath rapid breathingchest tightness Pathophysiology of asthma (5) -airway inflammation, bronchial hyper-reactivity and smooth muscle spasm -excess mucus production and accumulation -hypertrophy of bronchial smooth muscle -airflow obstruction -decreased alveolar ventilation Bronchioles smaller passageways that originate from the bronchi that become the alveoli 3 layers of the bronchioles innermost layer middle layer - lamina propria outermost layer lamina propria the middle layer of the bronchioles structure of the lamina propria embedded with connective tissue cells and immune cellspurpose of the lamina propria white blood cells are present to help protect the airways How does the lamina propria effect the lungs in regards to asthma the WBCs protective feature goes into overdrive causing an inflammatory response that damages host tissue What does the innermost layer of the bronchioles contain columnar epithelial ells and mucus producing goblet cells What does the outermost layer of the bronchioles contain smooth muscle cells what does the outermost layer of the bronchioles do control the airways ability to constrict and dilate alveolar hyperinflation When air is unable to move out of the alveolar like it should due to bronchial walls collapsing around possible mucus plug thus trapping air inside how does hyperinflation occur?the ongoing inflammatory process of asthma produces mucus and pus plug that the bronchial walls collapse around Effect of hyperinflation of the alveolar -expanded thorax and hypercapnia (retention of CO2) - respiratory acidosis What are two anticholinergic drugs used for asthma tiotropium and ipratropium What do anticholinergics do in the lungs? These drugs block the effects of the parasympathetic nervous system - increasing bronchodilation MOA of anticholinergic drugs for asthma the parasympathetic system is stimulated by the vagal nerve to release acetylcholine which binds to the cholinergic receptors of the respiratory tract to cause bronchial constriction = decreased airflow - blocking the cholinergic receptors prevents acetylcholine binding preventing the bronchial constriction bronchitis inflammation of the bronchial tubes3 characteristics of bronchitis bronchial inflammation hypersecretion of mucus chronic productive cough for at least 3 consecutive months for at least 2 successive years Perfusion The supply of oxygen to and removal of wastes from the cells and tissues of the body as a result of the flow of blood through the capillaries. results of chronic bronchitis/ low perfusion cyanosis right to left shunting chronic hypoxemia Why is there cyanosis with chronic bronchitis there is hypoxia due to unfavorable conditions for gas exchange Right to left shunting when blood passes from the right ventricle through the lungs and to the left ventricle without perfusionCauses of bronchitis -long term exposure to environmental irritants -repeated episodes of acute infection (RSV infection in early infancy) -Factors affecting gestational childhood lung development (preterm birth) Pathogenesis of bronchitis -Exposure to airborne irritants - Irritant activates bronchial smooth muscle constriction and mucus secretion - Triggers release of inflammatory mediators from immune cells located in the lamina propria most common irritant with bronchitis is? tobacco product smoke what does long term exposure to irritants promote in bronchitis? (5) - smooth muscle hypertrophy - hypertrophy and hyperplasia of goblet cells - epithelial cell metaplasia - migration of more WBC to site - thickening and rigidity of bronchial basement membrane What does smooth muscle hypertrophy do in lungs? causes increased bronchoconstrictionHypertrophy and hyperplasia of goblet cells do what in the bronchials promotes hypersecretion of mucus What are characteristics of epithelial cell metaplasia? squamous cells become nonciliated and are less protective; allow passage of toxins and WBCs What does the migration of WBCs to the bronchials do? increases inflammation of the cite and causes fibrosis in the bronchial wall How does the thickening and rigidity of bronchial basement membranes effect the lungs? leads to further narrowing of the bronchial passageways What acid-base disorder is seen in chronic bronchitis? respiratory acidosis how does chronic bronchitis lead to respiratory acidosis? hyperinflation of the alveoli causes CO2 retention Where does air enter the body? naso and oropharynx (mouth and nose)Where does air go after it passes through the nose and mouth? it passes through the trachea After air passes through the trachea where does it go? goes into the left or right bronchi Where does air flow after the bronchi? into the smaller bronchioles Where does air flow after the bronchioles? into the alveoli Describe how blood flows to become oxygenated - deoxygenated systemic blood flows from the vena cava to R atrium - Tricuspid valve opens to flow to R ventricle -Pulmonary semilunar valve opens and blood flows to the alveolar capillaries for gas exchange from the pulmonary trunk and L & R pulmonary arteries - blood goes from alveolar capillaries to pulmonary veins to return oxygenated blood to the left atrium - bicuspid valve opens to allow blood to go to left ventricle - aortic semilunar valve opens and blood goes to the aorta - aorta pushes oxygenated blood out to the bodyWhat is the formula for cardiac output CO = HR x SV cardiac reserve difference between resting and maximal CO; should be about 4-5x as high but does decrease 1% per year after age 30 What type of relationship does heart rate and stroke volume have? inverse low HR = longer fill time = increase stroke volume high HR = lower fill time = lower stroke volume What is preload? the degree of stretch on the heart before it contracts/ amount of blood entering the ventricles during diastole average amount of preload? 120-130 mls When fibers stretch during diastole how does that effect contraction? contraction is strongerWhat happens when cardiac fibers overstretch during diastole? decreased contraction due to fibers being unable to snap back What can cause increased preload CHF and hypervolemia What can cause decreased preload cardiac tamponade and hypovolemia What are two common causes of hypovolemia dehydration and hemorrhage Afterload the amount of resistance to open the semilunar valves and eject of blood from the ventricle what influences afterload (3) ventricle wall thickness (muscle strength) arterial pressure (resistance to ejection) ventricle chamber size (blood volume capacity) what can cause an increase in afterloadsystemic hypertension valve disease COPD (pulmonary hypertension) what can decrease afterload hypotension or vasodilation what influences cardiac contractility (inotropic state) levels of electrolytes High levels of ATP level of oxygen available synchronous muscle contraction What electrolytes are used for cardiac muscle contraction? sodium potassium and calcium What increases cardiac muscle contraction sympathetic stimulation; fear anxiety and increased thyroxine what decreases cardiac muscle contraction low ATP levels; ischemia hypoxia or acidosisStimulation of what set a resting HR (chronotropic state) parasympathetic system what stimulates the parasympathetic system the vagus nerve What does the parasympathetic system do? It releases acetycholine which decreases heart rate and causes vasodilation What can extreme vagal response result in? life threatening bradycardia What mediates the sympathetic system epinephrine and norepinephrine What does the sympathetic system promote in the cardiac system vasoconstriction and increased HR What can uncontrolled tachycardia lead to? reduced stroke volume and fatigueWhat are the two parts of the cardiac cycle? diastole and systole What causes blood to move from the atria to the ventricles gravity and atriole systole What causes the S1 heart sound? Bicuspid/Mitral and Tricuspid valves closing What are the atrioventricular valves? tricuspid and bicuspid (mitral) valves What are the semilunar valves? pulmonary and aortic valves What causes the semilunar valves to open? As ventricles contract and intraventricular pressure rises, blood is pushed up against the SL valves, forcing them to open ejection fraction measurement of the volume percentage of left ventricular contents ejected with each contractionWhat causes the semilunar valves to close? ventricles relax and intraventricular pressure falls, blood flows back from the arteries, and fill the cusps of the semilunar valves What causes the S2 heart sound? closing of semilunar (aortic and pulmonary) valves What prevents the backflow into the ventricles semilunar valves Stenosis of heart valve A narrowing of the valve opening, causing turbulent flow and enlargement of the emptying chamber Stenosis of a heart valve, may result in what? Narrowing of the heart valves means that blood moves with difficulty out of the heart. Results may include chest pain, edema in the feet or ankles, and irregular heartbeat. and hypertrophy heart failure cardiac dysfunction caused by the inability of the heart to provide adequate CO resulting in inadequate tissue perfusionLeft sided heart failure characteristic inability of the left ventricle to provide adequate blood flow into systemic circulation Causes of left sided heart failure systemic hypertension left ventricle MI LV hypertrophy Aortic SL valve or bicuspid valve damage Secondary to right heart failure How does LV hypertrophy lead to left sided heart failure The hypertrophy is secondary to cardiac damage resulting in an enlarged by weaker structure that holds more blood How does Aortic SL valve or bicuspid valve damage lead to heart failure damage leads to back flow into the left atrium or ventricle after ejection Biventricular failure unresolved left sided heart failure will increase pressure on the right side of the heart contributing to right sided heart failure as well How does heart failure progress from hypertension?- high systemic vascular pressure causes high after load requires the left ventricle to increase contraction force to eject the blood - damage causes reduced ejection fraction and left ventricle gets tired and becomes unable to eject normal amount of blood - increased amount of blood remaining in left ventricle and increased left ventricle preload causes the left atrium unable to eject the normal amount of blood into the left ventricle - blood volume and pressure backs up into the pulmonary veins - increased pressure will force fluid from the pulmonary capillaries into the pulmonary tissues What does fluid in the pulmonary tissue result in the areas are flooded and results in pulmonary edema and dyspnea cor pulmonale right-sided heart failure right sided heart failure inability of the right ventricle to provide adequate blood flow into the pulmonary circulation Causes of right sided heart failure- pulmonary disease - pulmonary hypertension - RV MI - RV Hypertrophy - pulmonary SLV or tricuspid valve damage - secondary to left heart failure What is the most common cause of right sided heart failure pulmonary hypertension Progression of right sided heart failure - damage causes the right ventricle to increase contraction force to eject/unload the blood - over time EF is reduced and right ventricle us unable to eject the normal amount of blood - the blood remaining in the RV increases and RA preload increases until the RA is unable to eject the normal amount of blood into the RA - the amount of blood remaining in the right atrium increases causing an increase in RA preload - blood volum enad pressure then backs up into the vena cava and systemic veins signs and symptoms of right sided heart failurejugular vein distension hepatosplenomegaly peripheral edema Why does hepatosplenomegaly develop in right sided heart failure the large volume of blood flow through the liver and spleen causes these areas to be engorged why does peripheral edema occur in right sided heart failure Increased pressure forces fluid from the systemic capillaries into the peripheral tissues and flood those areas High output failure inability of the heart to pump sufficient amounts of blood to meet the circulatory needs of the body despite normal blood volume and cardiac contractility causes of high output failure Severe anemia Nutritional deficiencies Hyperthyroidism Sepsis Extreme febrile state Process of high output failure- impaired oxygen delivery of excessive tissue oxygen demands cause tissue hypoxia - catecholamines initiation increase HR and stroke volume - increased cardiac output is produced but depletes cardiac muscle reserve overtime and leads to low output failure over time Troponin-Calcium Binding Calcium binds to troponin on the thin filament sliding filament theory theory that actin filaments slide toward each other during muscle contraction, while the myosin filaments are still Hematopoiesis formation of blood cells Where does blood cell formation occur in a fetus 3 weeks - yolk week 8 - fetal liver and spleen 5th month - bone marrow Blood cell formation in chidren 0-5 years old red marrow of all bones to make blood cells blood cell formation in adults over 20 red marrow in large bones -illium, vertebrae, cranium, jaw, sternum, ribs, humerus, and femurErythropietin Produce: Kidney (small amount in liver) Released: Kidney Target: Bone Marrow Functions: Stimulates bone marrow to produce more red blood cells hematopoietic stem cells The stem cells that give rise to RBC WBC and platelets through the process of haematopoiesis. How does a hematopoietic stem cell produce a red blood cell hematopoietic stem cells produces an unndifferentiated hemocytoblast - erythropoietin binds to it and createsa a proerythroblast - cell develops into an erythrocyte 7 days later Erythrocyte function transport oxygen and carbon dioxide Erythrocyte life span 120 days anemia risk factors acute or chronic blood loss, increased hemolysis, inadequate dietary intake or malabsorption, bone marrow suppression, age function of hemoglobin In red blood cells, carries oxygen from the lungs to body's tissues and returns carbon dioxide from tissues back to lungs. It also maintains the shape of red blood cells. causes of anemia - impaired RBC production - excessive blood loss - increased RBC destruction hemolytic anemia premature destruction of RBCs causes of hemolytic anemiainfection transfusion reaction hemolytic disease of the newborn (Rh incompatibility) autoimmune reaction drug induced development of anemia due to gastrectomy loss of intrinsic factor from surgery results in the loss of protein necessary for vitamin B12 absorption an can lead to anemia what kind of anemia can result from incorrect blood transfusion hemolytic anemia normocytic normochromic anemia Characterized by red cells that are relatively normal in size and hemoglobin content but insufficient in number hemolytic anemia is what kind of anemia normocytic normochromic anemia polycythemia vera condition characterized by too many erythrocytes; blood becomes too thick to flow easily through blood vessels Kidney Anatomy renal artery renal vein cortex, medulla, renal pelvis ureter renal pyramid nephron Nephron Anatomy 1. glomerulus 2. bowman's capsule 3. collecting duct 4. tubule 5. capillary Bladder anatomy - ureter - bladder -urethra reabsorption (kidney)movement of solutes from filtrate to blood things taken back that were secreted of filtered by the kidney what solutes are typically reabsorbed glucose, ions, amino acids and urea Where is most of the solute reabsorbed? proximal convoluted tubule What effects amount of water and solute reabsorption ADH and aldosterone secretion (kidney) movement of solutes from blood to filtrate anywhere besides bowman's capsule able to secrete salts, acids, bases and urea directly into the tubule via active or passive transport what is secreted into the tubule depends on what the body needs at that time ex. eating a lot of protein nitrogen waste is a product of protein metabolism (ammonia) liver converts ammonia to urea and the kidneys secreted urea into the tubule for secretion also possible to eliminate products that are in excess in the blood -- potassium, hydrogen, metabolites or medications can secrete things that were too larger to fit through the glomerulus's pore filtration (kidney) movement of solutes from blood to filtrate at bowman's capsule 20% of the blood that goes through the glomerulus is passed as filtrate into the bowman's capsule depends on the hydrostatic and oncotic pressures/ starling forces between the glomerulus and bowman's capsule hydrostatic pressure: a lot higher in the glomerulus (move into the nephron/bowman's capsule)oncotic pressure: higher in the blood/glomerulus than in the bowman's capsule (move into the blood/glomerulus) hydrostatic pressure is greater so there will be movement into bowman's capsule usually favors the filtrate to go into the bowman's capsule each persons full body is filtered about every 40 minutes Conditions associated with renal failure - congenital abnormalities in the urethral tract development - kidney and bladder cancer - infections - glomerulonephritis - acute/ tubular necrosis - AKI vesicoureteral reflux Abnormal ureter-bladder connection allowing retrograde flow of urine from bladder to ureters and/or kidneys renal agenesis unilatral or bilateral failure of the kidneys to develop in utero Potter syndrome Syndrome characterized by bilateral renal agenesis and incompatibility of live birth Wilms tumor - Embryonal kidney tumor associated with defective tumor (WT) genes - Tumors are typically not clinically diagnosable until age 1-5 even though they are present at birth polycystic kidney disease - Mutant PKD genes cause fluid accumulation in kidney tubules "cysts" - The cysts can be the size of grapes or oranges and compress and destroy nephrons Why are kidneys and bladders at high risk for cancer - UT is the route of excretion for many toxins and contains highly mitotic cells Descending infectionThe blood can carry bacteria from a focus of infection in another part of the body to the kidneys. The bacteria then pass with the urine down the ureters to the bladder. Ascending infection - urethra to bladder, and then to kidney - due to: bacteria from residual fecal contamination glomerulonephritis inflammation of the glomeruli of the kidney tubular necrosis the renal tubules cells are highly sensitive to low oxygen levels or presence of toxins and leads to tubular necrosis Causes of tubular necrosis - being post operative - severe sepsis - burns - trauma - contrast chemical use in medical imaging procedures Pathophysiology of tubular necrosis - ischemia or nephrotoxin exposure occurs to the renal tubules - inflammation and tubular injury occur - cast formation and tubular obstruction occurs - tubular injury, leakage, increased glomerular pressure causes decreased capillary perfusion further decrease in GFR occurs - oliguria results Acute Kidney Injury Sudden decline in kidney function with a decrease in GFR and an increase in plasma creatinine and BUN levels -results in oliguria Prerenal disease decreased blood flow to and through the kidney prerenal disease causes - hypotension - decreased cardia output - decreased blood volume What are most cases of AKI caused by?prerenal issues Intrarenal disease disease or damage within the kidney Causes of intrarenal disease ATN Acute glomerulonephritis postrenal disease obstruction in the lower urinary tract that prevents urine flow from the kidneys Causes of postrenal disease BPH Calculi Inflammation Tumors Chronic kidney disease progressive, irreversible deterioration in renal function Labs: elevated BUN, Cr Phosphorus. Rx: meds for hypertension, statins, epoetin, diuretics, calcium, LOW protein, low salt, restrict K, phosphorus (no chicken, milk, legumes, carbonated drinks), dialysis. kidney stones Solid crystalline masses formed in the kidney, resulting from an excess of insoluble salts or uric acid crystallizing in the urine; may become trapped anywhere along the urinary tract. kidney stone treatment high fluid intake, decreasing dietary intake of stone-forming substances, stone removal causes of kidney stones Family HX, chronic dehydration and infection, dietary factors, medications, imobility. Stoned more common in men than women usually ages 30/50. benign prostatic hyperplasia benign growth of cells within the prostate gland BPH (benign prostatic hyperplasia) Age-associated prostate gland enlargement that can cause urination difficulty.BPH treatment - Alpha-adrenergic antagonists: terazosin, doxazosin - 5-alpha reductase inhibitors: finasteride, dutasteride - Transurethral prostatectomy - Open prostatectomy pathogenesis of primary glomerulonephritis - infection triggers of immune response to cause formation of antibodies - antibodies form complexes with the pathogen that should be rapidly phagocytized by WBC - in glomerulonephritis the Ag-Ab complexes are not phagocytized in a timely manner and continue to circulate in the blood stream - the Ag-Ab complexes get trapped in the narrow vasculature of the glomerular capillaries - build up of the Ag-Ab complexes signals that immune system and the complement system and WBC infiltration of the site - Complement protein with enzymes released by phagocytic cells attack the complexes and cause collateral damage to the glomerular area - Damage weakens thee glomerular structure and plasma proteins with blood leak into the tubular system and pass out into the urine clinical indicators of glomerulonephritis - proteinuria - hematuria - edema - azotemia - oliguria - coagulation cascade activation Why is there edema with glomerulonephritis the loss of albumin from the bloodstream reduces plasma oncotic pressure and results in edema Azoetmia presence of elevated plasma creatinine Why is there azoetmia with renal failure? Decreased GFR means waste is remains in the bloodstream and is not excreted Why is there oliguria with renal failure?when the glomerual structure has sustained enough damage the nephron structure is no longer functional as a filtration unit What happens in renal failure when the coagulation cascade is activated fibrin is deposited in the glomerular structure and decreases capillary perfusion by causing blockages and further decreases GFR further blood hydrostatic pressure the pressure produced by a fluid against a surface filtration (kidney) movement of solutes from blood to filtrate at bowman's capsule 20% of the blood that goes through the glomerulus is passed as filtrate into the bowman's capsule depends on the hydrostatic and oncotic pressures/ starling forces between the glomerulus and bowman's capsule hydrostatic pressure: a lot higher in the glomerulus (move into the nephron/bowman's capsule) oncotic pressure: higher in the blood/glomerulus than in the bowman's capsule (move into the blood/glomerulus) hydrostatic pressure is greater so there will be movement into bowman's capsule usually favors the filtrate to go into the bowman's capsule each persons full body is filtered about every 40 minutes angiotensin converting enzyme (ACE) an enzyme that converts angiotensin I to angiotensin II What does angiotensin II do? increases blood pressure by vasoconstriction Role of macrophages -In Innate: 1. Phagocytosis PRR or opsonization w/ complement2. Secrete Cytokines: Recruit more cells, inflammation, fever, etc. -In Adaptive: 1. Phagocytosis: opsonization with complement or Abs 2. Secrete cytokines: recruit more cells etc. 3. Antigen presentation: peptides from the broken down pathogen are displayed on surface of the cell.