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COMPLETE Pathophysiology Notes - Part 1 (4.0ed the final exam!)

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Boston College
NURS 2080

CARDIOVASCULAR ALTERATIONS Terminology Laminar v. turbulent flow Laminar: smooth blood flow, they way it should be (RBCs should barely touch vessel wall) Turbulent: occurs in cardiovascular diseases Can initiate platelet responses – clotting cascade initiated Systole v. diastole Systole: filling Diastole: filling Afterload v. preload Preload: volume of blood in ventricles at end of diastole (end diastolic pressure); right side of heart – stretch on heart (left v. right); filling pressure Afterload: resistance LV must overcome to circulate blood Hypertension constricts aorta Peripheral vascular resistance: sum of the resistance of all peripheral vasculature in systemic circulation Arrhythmias Supraventricular v. ventricular Supraventricular: arrhythmias initiated above ventricles Ventricular: arrhythmias originated in vesicles Hyperlipidemia: a risk factor for CV disease We need lipids because they produce many hormones and are main part of cell membrane Lipoproteins: we need them because cholesterol and triglycerides cannot travel through body themselves HDL (high density) Good cholesterol Takes up excess cholesterol and brings to liver; reverse cholesterol transport; once in liver it is eliminated in bile or made into steroids LDL (low density) Bad cholesterol; carries mostly cholesterol VLDL (very low density) Mostly carries triglycerides Elevated LDL (“bad cholesterol”) Strong indicator of coronary risk Role in endothelial injury, inflammation & immune responses Low levels of HDL strong indicator of coronary risk HDL Responsible for “reverse cholesterol transport” Participates in endothelial repair & decreases thrombosis Increased VLDL and lipoprotein A elevate risk VLDLs carry triglycerides Not tested on lipoprotein A Elevated total cholesterol Bad: combination of all (sum of LDL, HDL, and VLDL) Good: Just elevated HDL Causes Can run in family; or diet issue (lots of saturated fat); medications; diabetes mellitus Atherosclerosis: formation of fibrous fatty lesions of intimal lining of arteries *Atherosclerotic plaques can occur in any artery (i.e. coronary, cerebral, aorta, peripheral arteries, etc) Risk factors Non-modifiable: increase risk of atherosclerosis development Genetics Gender (typically male gender until post-menopause) Increasing age Hyperlipidemia (if genetic cause) African American race Modifiable (can change) Diet (hyperlipidemia (due to diet) and elevated LDL) Diabetes mellitus Obesity Hypertension Smoking – elevates BP and sympathetic stimulation Nontraditional C reactive protein (CRP) elevation CRP is a marker of systemic inflammation Baseline CRP can predict future CV events among healthy patients Hyperhomocystinemia Homocystine: metabolism of amino acid methionine (found in animal protein) Can inhibit anticoagulant cascade Associated with endothelial damage Increased Lipoprotein A (not tested on) Lipoprotein A = altered form of LDL Enhances cholesterol delivery to injured blood vessels Suppresses generation of plasmin (fibrinolytic enzyme) Promotes smooth muscle proliferation Complications (because arteries are hardening; lesions depositing in vessels cause a narrowing) Ischemia (pain resulting from lack of oxygen/low levels) Caused by partial occlusion Complicated lesion w/obstruction Thrombus & emboli Clot formation can lead to thrombosis Aneurysm Assessment Pain (infarction  no oxygen  cell death  pain) Chest pain In PAD, pain will be in affected extremity Arterial bruits (turbulent flow through a vessel; heard with bell of stethoscope) Development Endothelial cell (lining of vessel walls) injury and migration of inflammatory cells Endothelial injury risk factors High LDL levels Hypertension (creates turbulent flow) Smoking (vasoconstriction  turbulent flow) When endothelial cell breaks, monocytes migrate between endothelial cells (leave circulation) and become macrophages Macrophages release cytokines and mediators including oxygen radicals (allows macrophage to eat excess LDL) After consuming LDL, macrophage becomes a foam cell Foam cell = basis of lipid core of plaque Lipid accumulation & smooth muscle cell proliferation New smooth muscle cells come to scene to replace damaged cells; healing of smooth muscle Foam cells full of lipids; elevation in lumen of vessel Fibrous atheromatous plaque Gray or white, elevated thickening Size increases & occludes vessel Lesions (necrotic core forms from accumulation of foam cells – anytime necrosis occurs it is vulnerable to rupture because cap becomes weak) Unstable plaque: fibrous cap becomes weak/unstable (# foam cells under cap contributes) Complicated lesion: thin fibrous cap breaks; whole response occurs again (i.e. more platelets) Initiation of clotting cascade: blood clot forms (can possibly occlude vessel) Peripheral Arterial Disease (PAD) Plaques occurring in lower extremities (anything below distal arch of aorta) Risk factors Smoking Diabetes Symptoms (Gradual symptoms because gradual narrowing of vessel) Intermittent claudication = biggest complaint Intense calf pain after taking a walk; sit down and rest; pain goes away; pain returns with walking Has to do with gastric nemous muscle (has high affinity for oxygen) Loss of subcutaneous fat/muscle loss Due to gradual narrowing of O2 supply to lower extremities Thinning of skin; leg hair loss (topical changes) Redness in leg when it’s dependent (i.e. sitting in bed) due to maximal arterial dilation Patients sit with legs hanging over bed so gravity gets blood flow to their legs Weak to no pulses in lower extremities  cool skin *With red skin, you would think leg would be warm but it’s cold Complications (from patients starving of oxygen) When disease worsens, intermittent claudication progresses into constant pain) Ulcerations (tissues die and skin turns black) Gangrene (dead tissue produces this) Aneurysms (abnormal outpunching of vessel from weakness in vessel wall) As it forms, it can impinge on other structures of body Risk factors (lead to progressive weakening and tension) HTN Atherosclerosis Chest trauma (i.e. hitting chest against steering wheel) Congential causes Types Berry: bifurcations Fusiform: circumferential Saccular: out-pouching on one side of vessel (sac-like appearance) Dissecting (a life-threatening emergency because it can easily burst) Vessels have 3 layers; break in innermost (intimal) lining of vessel; breaks into medial area Creates fluid-filled cavity between medial and intimal layer Aortic aneurisms Thoracic Atherosclerosis Usually asymptomatic Increasing size produces symptoms Impinging on lungs: shortness of breath/dyspnea Impinging on trachea: stridor Voice may become raspy Edema to face/anywhere above thoracic cavity Abdominal (abdominal aortic aneurysm: aaa; associated with severe forms) Half of people who develop this have HTN Most frequent 50 years of age Asymptomatic until impinges on structures 1 sign is pulsating mass in abdomen Pain if pressing on nerves Compressing lumbar nerve: pain could radiate to legs Emboli Risk factors decrease with a better diet and cessation of smoking Aortic dissection: hemorrhaging from intima layer into medial layer with longitudinal tearing Degeneration of medial layer vessel wall itself (tearing of intima layer – blood flows into media layer) Occurs in patients 40-60 years old Symptoms (important) Sheering, ripping, intense pain Could be chest or back pain Blood pressure is initially high and then plummets – sympathetic response Blood pressure (BP = CO x PVR) Blood pressure control is achieved by regulating it determinants Cardiac Output Calculated by stroke volume & heart rate PVR Reflects changes in radius of arterioles & viscosity Arterioles can constrict or relax selectively Arteries innervated by the sympathetic and parasympathetic pathways of ANS Baroreceptors sense changes in BP BP control: neural and humoral mechanisms Short-term neural mechanism (found in reticular formation of medulla and lower 3 of pons) Intrinsic reflexes for BP Baroreceptors (in carotid arteries; sense decrease in stress; increase PVR upon release) Stimulation  raised PVR  raised BP Chemoreceptors (mainly regulate ventilation; sense increase in CO2 and H+, sense low O2) Stimulation leads to raised BP Parasympathetic stimulation Vagal slows heart rate Sympathetic stimulation Increased HR & contractility Vasoconstriction Short-term humoral mechanism RAAS Renin persists 30 min - 1hour Released from sympathetic activity or when kidneys not getting enough blood Angiotensin II: converted in lungs Regulates aldosterone long-term Increases PVR Reabsorbs Na in proximal tubules Aldosterone Increases vascular volume by telling kidney to conserve salt and therefore water Vasopressin (antidiuretic hormone (ADH)): released from posterior pituitary Released when decreased circulating volume is sensed Increases PVR by vasoconstriction Instructs kidney to conserve water Adrenal gland releases epinephrine and norepinephrine Increase HR and contractility *Between renin and vasopressin vasoconstriction is caused (helps with BP) and fluid is conserved Long-term: Kidneys help regulate ECF by sensing circulating volume through pressure sensors Regulate blood pressure around an equilibrium point An increase in ECF Pressure diuresis Pressure natriuresis Natriuretic peptides help regulate urinary sodium excretion: pressure natriuresis = eliminating sodium Where sodium goes, water follows Released from heart when overstretched When body at equilibrium, kidneys stop with pressure and natriuretic diuresis Atrial natriuretic peptide (ANP) If atria overstretched, kidneys excrete sodium Brain natriuretic peptide (BNP) When ventricles overstretched, ventricular muscle releases BNP Hypertension Systolic and diastolic readings diagnosing hypertension Has rested for at least 5 minutes Has not smoked or ingested caffeine within 30 minutes Classifications Primary (essential) Non – modifiable risk factors (genetic cause) Family history Age African American Insulin resistance (i.e. diabetes – causes endothelial dysfunction over time  vasoconstriction) Modifiable risk factors Environment – diet (high salt intake) Obesity ETOH abuse (3+ drinks per day) Cigarette smoking Secondary – results from another disease process (only 5-10% of HTN cases) Renal HTN Renal disease Reno-vascular disease Renal flow & activation of RAAS Adrenocortical Primary hyperaldosteronism = excess fluid  high BP Cushing Disease; glucocorticoids contribute to high BP Pheochromocytoma Cancer of adrenal gland; catecholamines (epi, norepi) produced Catecholamines  vasoconstriction, HTN Drugs – BP pills, cocaine *huge sympathetic stimulator If fix cause with secondary, BP will go back down Target organ damage Cardiovascular HTN leading risk factor for cardiovascular disorders Systolic elevation Left ventricular hypertrophy CHF Cardiac arrhythmias Sudden death Elevated Pulse pressures Stretch to arteries cause elastic vessel damage Aneurysms Atherosclerosis CAD (coronary artery disease) PAD (peripheral artery disease) Thrombosis formation Kidney Nephrosclerosis Progressive damage to vessel & arterioles leading to ischemic death of nephrons Accelerates other types of kidney disease Diabetic nephropathy Brain Stroke High BP causes dilation of small noneslastic vessels (very fragile) leading to hemorrhage Ischemic stroke Dementia Narrowing & sclerosis leads to hypoperfusion  probable cause of white matter demyelination Caused by constant vasoconstriction – less blood flow going to areas of brain, causes this demyelination Eye Retinopathy (from constant stress on vasculature) Hypertensive crisis Associated with Secondary Hypertension (usually causes extreme elevation of BP) Hypertensive emergency Diastolic greater than 120 Rapidly progressing Target organs damaged Brain (turbulent blood flow through fragile vessels; constant hydrostatic pressure; edema) Spasm of cerebral arteries with hypertensive encephalopathy Headache Restlessness Motor & sensory deficits Visual disturbances from pressure on optic nerve Stroke Hypertension in elderly Prevalence increases with age Aging process Stiffening of large arteries Increased PVR Decreased renal blood flow Decreased baroreceptor sensitivity Treatment medications are initiated at smaller doses Orthostatic hypotension (postural hypotension) Abnormal drop in BP upon standing Causes Reduced blood volume (blood loss) Drug induced Aging (decreased skeletal pumps) Normally, skeletal pumps in legs push blood flow up to superior vena cava) Sympathetic response is slower in elderly Bed rest & immobility (can affect venous vasculature) Symptoms = light-headedness, syncope Chronic venous insufficiency Venous HTN (increased pressure within veins; can be due to incompetent veins and valves) Signs – Impaired blood flow Edema Hyperpigmentation (brown; due to tissue congestion and breakdown of RBCs Necrosis of SQ fat deposits Advanced disease - impaired tissue nutrition Stasis Dermatitis (bluish color within legs due to lack of subcutaneous tissue support) Venous ulcer (when thin skin breaks open) Outflow obstruction – deep vein thrombosis (partially occludes vessel) Due to tissue congestion, the ulcers are wet and leaky (exudate pushed into interstitial areas from hydrostatic pressure); legs are full of fluid Venous thrombosis (DVT) Thrombosis of vein with inflammatory response in vessel wall Inflammatory response allows clot to grow once it forms Symptoms Swelling of foot, ankle, or calf Tenderness Pain Complication: pulmonary embolism (clot can break off and end up in lungs) Age-related changes Myocardial and blood vessel stiffening Vascular media changes Contributor to systolic HTN, Risks for CV events (strokes), dementia Changes in neurogenic control over vascular tone Catecholamine receptor sensitivity Baroreceptor activity decreases with age Increased peripheral vascular resistance & decreased renal blood flow Antihypertensive medication in smaller doses Left Ventricular Hypertrophy & Fibrosis Disruption of growth factor Imbalance in collagen synthesis & degradation BLOOD CLOTTING AND ABNORMALITIES Leukocytes (WBCs) Thrombocytes (platelets) Erythrocytes (RBCs) Plasma – fluid that all blood cells and platelets are suspended in All cells derive from a single pool of pluripotent stem cells of bone marrow Lymphoid stem cells Myeloid stem cells Growth & reproduction of blood cells Hematopoiesis = production and development of blood cells, normally in bone marrow Growth Factors (hematopoietic growth factors) Stimulate committed hematopoietic progenitor cells EPO – erythropoietin (hormone)*** Tells bone marrow to make more cells – released by kidneys GM-CSF – granulocyte-monocyte colony stimulating factor Stimulates granulocytes, monocytes, erythrocytes & megakaryocytes Interleukin-3 – growth factor for progenitor hematopoietic cells Proliferation of stem cells and development of lymphocytes Interferons & tumor necrosis factor Erythrocytes Biconcave disk Greater SA for oxygen diffusion Flexibility Hemoglobin Carries oxygen to body tissues Iron gives RBCs red color Blue when deoxygenated Iron needed for HGB synthesis 65% of iron is in the form of HGB Iron is recycled Diet important Transferrin – iron circulating in blood Ferritin – iron stored in body tissues Life span 120 days Erythropoiesis Proerythroblasts Produced by pluripotent stem cells in bone marrow Precursor cells of RBCs 1 wk stem cell to reticulocyte Enters blood as reticulocyte Matures into erythrocyte in 24-48 hrs. High reticulocyte count indicates recent blood loss RBC production = destruction Hemoglobin higher in men than women (amount in blood) Hematocrit – if we take 100 ml plasma and measure it, it would measure RBC mass within plasma If you have hypochromic (less hemoglobin) blood – less cells, seen in iron deficiency anemia – lighter color of cells Anemia – abnormally low # circulating RBCs, or low hemoglobin Diminished O2 capacity  tissue hypoxia Symptoms Pallor – white color Weakness, fatigue Respiratory Central nervous symptoms – fainting, dizziness Appearance of manifestations Slow developing – symptoms might not appear until 50% blood loss Mild Acute – may lead to cardiovascular collapse from fluid loss ***OVERALL, our tissues are not getting as much oxygen as they need, so we have diminished O2 capacity which can lead to tissue hypoxia (when talking about anemia, tissue hypoxia leads to weakness and fatigue)*** Anemia of acute blood loss 10-20% of blood loss can occur before symptoms Volume loss causes a decrease in venous return Low BP, decreased CO & decreased central pressure Diverts blood to vital organs kidney RAS conserve salt & H2O Sympathetic nerve activation  blood vessels constrict 20-30% loss – no significant symptoms Tachycardia, slight postural hypotension 40% loss – rapid thready pulse Cold clammy skin 50% loss – shock and potential death 5 days for progeny of hematopoietic stem cells to differentiate fully RBC count returns to normal 3-4 weeks (need adequate iron stores) When less blood back to superior vena cava - body stimulates sympathetic system Constricts vessels to allow more blood to go back to superior vena cava and right side of heart Sensors sense where there is low BP Blood flow to periphery is shunted (less to feet and hands) BUT blood is also shunted from kidneys Kidneys sense that they’re not getting enough blood and they release renin and begin RAAS Aldosterone conserves salt and water Acute blood loss also causes tachycardia from the sympathetic stimulation BUT blood loss causes low BP As a nurse, picking up on high heart rate and low BP ---- anemia Hemolytic anemia Premature destruction of RBC HGB in plasma Iron retention Can be excess iron circulating (because it’s supposed to be in RBC) Heme pigment in plasma Parts of RBC circulating in periphery – heme, iron Causes Intrinsic – hereditary (sickle cell anemia is a form of hemolytic anemia) Extrinsic – mechanical trauma, incompatible blood transfusion reaction, infections S&S Easy fatigability (from tissue hypoxia), dyspnea, increase rate & depth (compensation) Jaundice (from breakdown of HGB) Lab Normocytic & normochromic cells Increased reticulocyte count (body making more RBCs) Sickle cell anemia Inherited recessive disorder of an abnormal HGB Sickle cell trait (inherited one HbS gene) Sickle cell disease (inherited two HbS genes) HbS sickles/polymerizes when deoxygenated  semi solid gel (rather than nice circle) Repeated occurrences irreversibly sickle cell Gets stuck in some tissues; no longer biconcave flexible disk Results in: Chronic hemolytic anemia Blood vessel occlusion Tissue ischemia (possibly inflammation in addition) Pain Factors associated with sickling & occlusion Cold (stimulate cells to sickle) Stress Physical exertion Infection Illness causing hypoxia (ex: pneumonia) Dehydration Acidosis Complications Vaso-occlusive pain Acute chest syndrome Sickling within chest cavity  shortness of breath and fever Prone to infections Filtering ability decreased; more susceptible to pneumonias Iron-deficiency anemia Microcytic-hypochromic anemia Decreased O2-carrying capacity Causes Dietary deficiency Increased iron demands Children going through growth spurts Pregnant women Loss of iron from bleeding Symptoms Fatigue, pallor Waxy pallor syndrome; skin looks waxy and white (tongue can look shiny) Spoon-shaped nails Patients may eat dirt, maybe ice Lab Low iron & ferritin levels Low HGB & HCT MCV & MCHC Small, pale cells Pernicious anemia (B12 deficiency) Megaloblastic anemia (large cells) Has to do with extracytoplastic growth Disorders Associated with: Gastric/Stomach Terminal ileum Symptoms – usual anemia symptoms Changes on mucosal cells Neurologic deficits (numb, tingling fingers and toes) Diagnosis and treatment CBC – elevated MCV, normal color & reticulocyte count Low B 12 levels Parietal cell & intrinsic factor antibodies *B12 needed for DNA synthesis and nuclear maturation to produce normal mature cells & normal cell division, and to prevent myelin breakdown Intrinsic factor binds vitamin B12 and transports it into ilium of intestines –-> crosses over in portal vein  B12 stored in this vein in liver for use *Intrinsic factor produced by parietal cells Destruction of these cells (i.e. an autoimmune disorder, cancer of stomach)  perniciou
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