N112 Unit 2 PDF

CHAPTER 21: DISORDERS OF OXYGEN TRANSPORT Red blood cell disorders involve loss of oxygen in tissues and loss of mature erythrocytes Genetic variation ○ Prevents formation of mature erythrocytes or hemoglobin ○ Misshapen erythrocytes cause cells to clump together and can cause ischemia or hypoxia Ex...

CHAPTER 21: DISORDERS OF OXYGEN TRANSPORT Red blood cell disorders involve loss of oxygen in tissues and loss of mature erythrocytes Genetic variation ○ Prevents formation of mature erythrocytes or hemoglobin ○ Misshapen erythrocytes cause cells to clump together and can cause ischemia or hypoxia Excessive RBCs cause blood to thicken Anemia is a common clinical condition that involves a reduction in the # of erythrocytes and decline in ability of to carry oxygen Decreased production of erythrocytes, loss of erythrocyte (acute of chronic blood loss) Reduced survival time of erythrocytes Functional changes in structure of erythrocytes Also involved nutritional deficit → production of RBCs is decreased because lack of necessary components for synthesis of DNA = continued cell growth with lack of appropriate cell division Macrocytic anemia - vitamin B12 and folic acid Iron deficiency anemia and thalassemia - iron Aplastic anemia involves a reduction in stem cells Other causes include medication and radiation of anemia of chronic disease Clinical manifestation involve fatigue (most common), increased respiration and heart rate (to compensate), pallor, cyanosis (usually not), headache and dizziness, muscle weakness Hypoxia effects on body Dilation of arterioles, capillaries, and venules to increase blood flow → increases heart rate and stroke volume, can lead to heart failure Rate and depth of breathing increases in an effort to increase oxygen availability and also an increase in the release of oxygen from hemoglobin Diagnosis involves medical history, blood test, and identification of genetic cause Lab test can be used to classify anemia and identify cause or risk of anemia 13.5 - 17.5 g/ dL for men 12.0 - 15.5 g/ dL for women Treatment involves blood transfusion (if caused by blood loss), replacement of iron and vitamin B12 as needed, education (nonheme iron absorption is enhanced by animal protein a rich source of vitamin c) MCV reflect the average erythrocyte size Hematocrit Microcytic vs macrocytic anemia MCH Hypochromic Normochromic Nutritional deficiency anemia Hemolytic anemias Several nutrients are necessary for maturation and proliferation of RBCs Lack of iron and vitamin B12 affect cell maturation Hemolysis ( destruction) of RBCs Physical trauma and stress to RBC Disruption in hemoglobin formation Immune mediated response IRON DEFICIENCY Reduced dietary intake or malabsorption Chronic blood loss such as menstruation of GI bleeding Microcytic and hypochromic RBCs Major causes are genetic - sickle cell disease and thalassemia Signs and symptoms are similar to other forms of anime but it also include jaundice COBALAMIN DEFICIENCY Vitamin B12, a water soluble vitamin necessary for cell metabolism and binds to intrinsic factor secreted by gastric parietal cells once consumed Pernicious anemia ○ Autoimmune mediated process that lead to loss of gastric parietal cells -> decrease secretion of intrinsic factor -> inability to properly absorb cobalamin Autoimmune response ○ Can contribute to weakening the intestinal wall Bowel disease ○ Can adversely affect the absorption of cobalamin FOLIC ACID DEFICIENCY Obtained primarily through the consumption of fruits and leafy green veggies important for the synthesis and repair of DNA, work alongside cobalamin More chronic, insidious(dangerous and gradually) presentation Medication that antagonize folate can contribute to development of anemia For cancers, antibiotics Treatment inclined determining severity, monitoring or hematocrit and hemoglobin levels, blood transfusion, consideration for sickle cell disease SICKLE CELL DISEASE Cluster of autosomal recessive disorders Hemoglobin sickle or crescent in shape due to a genetic mutation Pathogenesis Hemoglobin cannot bind oxygen effectively RBC collapses into sickle shape when oxygen is released RBC clump together and can obstruct blood flow RBC lifespan is only 10-20 days (normal is 120 days) Chronic inflammation b/c inflammatory mediators are released in compensatory response to stimulate production of more RBCs Clinical manifestation include hypoxia and tissue ischemia Treatment includes: prevention, screening, supportive care (pain management), disease modifying strategies, curative procedures, genetic analysis and prenatal counseling Treatment may involve hydroxyurea for infants(stimulate production of hemoglobin), blood transfusion, stem cell transplantation THALASSEMIA Group of autosomal recessive disease the affect production of hemoglobin caused by a defect in the production of one or more globin chains Increase incidence in individuals from mediterranean and asia Clinical manifestation include: defects at birth, growth retardation, cognitive deficits, jaundice Anemia of chronic disease Aplastic anemia A condition of inflammation The process of inflammation is associated with the release of immune proteins that play a role in uptake and retention of iron In ACD, iron is taken up into macrophages, which divert it from being able to play a role in binding of oxygen Decrease in all cell population produced by the bone marrow: erythrocytes, leukocytes, platelets (body stops producing enough new blood cells) Caused include genetics, viral exposure, drugs or toxins, immune mediated attack on the bone marrow Diagnosis - decrease in WBCs, RBCs, platelets, hemoglobin Normochromic and normocytic b/c maturation of RBC has not been impacted, hyperproliferation Normocytic, normochromic Polycythemia vera is a bone marrow disorder Too many RBCs are produced → increase viscosity prevents blood from flowing efficiently, leading to end organ ischemia The increased thickness of the blood places the pt at an increased risk for the development of thrombi or blood clots Primary refers to an increase in the production of erythrocytes on the part of bone marrow while secondary results from genetic modification related to the production of erythropoietin, regulator of RBC production Clinical manifestation include: increase blood viscosity and volume, headache, dizziness, blurred vision, hypertension, thrombi Diagnosis include hematocrit over 70, increase erythrocytes and WBcs, decreased iron count Treatment includes anticoagulation, therapeutic erythropheresis (bloodletting), chemotherapeutic approaches CHAPTER 22: ALTERATION OF HEMOSTASIS Blood = plasma + formed elements (erythrocytes, leukocytes thrombocytes) Hemostasis is a term that refers to the cessation of blood flow, particularly through the action of coagulation (clotting) mechanisms Hemorrhage refers to copious bleeding which can be outside the skin (from laceration) or in the skin (ecchymoses) Disorders of hemostasis are related to excessive coagulation or excessive bleeding - disruption of homeostasis can occur at any point of coagulation 1. Vascular phase (initiation) a. Spasm of blood vessels (injury to blood vessel causes a reactive constriction of spasm of the blood vessels, and platelets are activated and travel to site) 2. Aggregation phase (amplification) a. Platelets form a plug (clump together) 3. Coagulation phase (propagation) a. Formation of fibrin (platelets release immune proteins+ forms film over platelet) Clotting is caused by intrinsic, extrinsic, and a common pathways Intrinsic Extrinsic Common Pathway Activated by trauma inside the vascular system Activated by platelets, exposed endothelium, chemicals, or collagen Activated by external trauma that causes blood to escape from the vascular system This pathway is much quicker Factor X is a vitamin K-dependent clotting factor and plays a central role in the coagulation cascade at the point of convergence of the intrinsic and extrinsic pathway Factors XII, IX, VII Factors VII, III Activated factor X causes a set of reaction resulting in the inactive enzyme prothrombin (factor II) being converted in the active form thrombin Thrombin then converts soluble fibrinogen (factor I) into insoluble fibrin strands The fibrin strands compromising the clots are then stabilized by factor XIII Clotting cascade is similar to the complement system and each enzyme of the pathway is present in the plasm in an inactive form The coagulation pathway is a series of + and - feedback loops that control the activation process with the end goal being to reduce thrombin Thrombin alters the structure of fibrinogen, transforming it into fibrin Fibrin provides a mesh like framework on which platelets can clump Cofactors include calcium, which serves to bind the clotting factors together for coagulation to occur while and vitamin K is essential for the functioning of several proteins involved in the regulation of blood clotting Both are required for the synthesis of protein c, an anticoagulant that prevents excessive coagulation after the coagulation cascade occurs. Deficiency of any of these clotting cofactors will cause an impaired ability for blood to coagulate and can contribute to excessive bleeding and hemorrhage Breaking down clots involves primary fibrinolysis, the body’s normal process and secondary fibrinolysis, caused by medication or disease process Plasmin is the main enzyme that cuts the fibrin mesh at various places Leads to the production of circulating fragments ○ Fibrin degradation produce ○ This number is reflected in the D-dimer D-dimer is a product of fibrin degradation that is present after blood clots are broken down. An elevated result may imply the presence of significant clotting propensity. Elevated levels can also be found in a number of other medical conditions and states. Plasminogen is the inactive from of plasmin produced in the liver ○ Required tissue plasminogen activator (T-PA) and urokinase to be converted to the active form of plasm ○ T-PA can be made in the lab and is known as recombinant r-PA Clot buster Various type of test for coagulation and bleeding D-dimer - fragment of fibrin degradation ○ D-dimer is a product of fibrin degradation that is present after blood clots are broken down. An elevated result may imply the presence of significant clotting propensity. Elevated levels can also be found in a number of other medical conditions and states. Activated partial thromboplastin time (aPTT) - same parameters as PTT, with clotting activator ○ Increased levels indicate prolonged bleeding. Particularly prolonged bleeding is associated with changes in the levels of select clotting factors, primarily factors II, V, IX, X, XI, and XII Fibrinogen - presence of soluble protein necessary for formation of fibrin Partial thromboplastin time (PTT) - functional ability of clotting pathway Vitamin k - vitamin essential to formation of several clotting factors Primary disorders Secondary disorders Associated with abnormalities in number or function of platelets Associated with lack of, or reduction in, factors tied to coagulation May occur as a result of genetic factors, liver dysfunction, dietary deficiency VON WILLEBRAND DISEASE Most common genetic bleeding disorder involving partial or complete deficiency in clotting factors (in which a lack of a certain factor prevents platelets from adhering to the site of injury, preventing the formation of a blood clot) Type 1 - most frequent and least severe, often asymptomatic Type 2 - some bleeding issues Type 3 - significant blood loss, internal bleeding, similar to hemophilia Treatments for spontaneous bleeding episode include desmopressin and transfusion with plasma derived vWF products THROMBOCYTOPENIA Most common cause of abnormal bleeding involving a decrease in number of circulating blood platelets Causes not well understood, infection and other inflammatory states. artifact, deficient production, increase destruction, consumption or both, abnormal distribution or pooling Clinical manifestation include purpura (easy or excessive bruising), ecchymoses, epistaxis (bleeding from nose), serious hemorrhages, petechiae (superficial bleeding into the skin that appears as a rash or pinpoint sized reddish purple spots, usually on lower legs) HEMOPHILIA Hereditary genetic bleeding disorder associated with the loss of select clotting factors and significant bleeding or soft tissues or joints Hemophilia A - factor VIII Hemophilia B - factor IX Can also be acquired from autoimmune disease, cancer, pregnancy Clinical manifestation (infants) excessive bleeding after circumcision (adults) severe mucosal bleeding from tongue or hum injuries, permanent bruising over trunk and extremities Lab test would should prolong PTT, normal PT, platelet counts, bleeding time, platelet function assays, Diagnosis involves analysis of factor VIII and IX activity Treatment involves episodic or prophylactic administration of factor VII or XI concentrates Treatment include plasmapheresis (plasma exchange), TTP therapy, infusion of fresh frozen plasma Issues of hypercoagulopathy in sickle cell disease Clinical manifestation include hypoxia and tissue ischemia Diagnosis involves increase concentration of thrombin with corresponding loss of anticoagulant proteins Treatment includes pharmacological treatments that reduce platelet binding and inhibit platelet activation Disseminated intravascular coagulation (DIC) is a life threatening condition that involves protein that control clotting becoming overreacting Causes include sepsis, shock, or damage to blood vessels ○ 3 can increase tissue factor and cause systemic activation of coagulation pathways Clinical manifestations - clots cause organ dysfunction, difficulty breathing, hemoptysis, tachycardia Diagnosis - low platelet and fibrinogen levels, prolongation of PT and aPTT results, with elevation in D-dimer values Treatment involves monitoring for blood loss and signs of organ failure due to ischemic damage or administration of platelet and other blood factors Patient education Patient who are at risk of excessive bleeding need to be educated about their condition and provided with instruction about preventing bleeding Bleeding precaution include using a soft toothbrush, wearing shoes at all times, avoiding contact sports, using stool softener to prevent straining CHAPTER 28: SHOCK AND MULTIPLE ORGAN DYSFUNCTION SYNDROME Hemodynamics = the force the heart has to respond to in order to maintain blood flow through the cardiovascular system and supply oxygen to ass tissues To have adequate perfusion, adequate cardiac output, a vascular system that is able to transport blood effectively, adequate circulating blood volume, and tissue that can extract oxygen effectively is needed Clinical signs of tissue hypoperfusion: cold clammy hands, renal output decreases, altered mental state. Obtundation discoloration confusion, hyperlactemia Shock involved acute circulatory failure with inadequate of inappropriately distributed tissue perfusion Inadequate tissue perfusion to meet metabolic needs of cells Cellular hypoxia and end organ dysfunction Imbalance between oxygen supplied and oxygen demands of cells → can lead to anaerobic metabolisms and lactic acid generation Inflammatory and clotting cascades Circulating alterations leading to shock: heart failure, low blood volume in circulation, redistribution of extracellular fluid to extravascular sites, obstruction of blood flow Blood pressure = cardiac output x systemic vascular resistance Types of shock 1. Hypovolemic shock (hemorrhagic shock) - rapid blood or other ECF fluid loss 2. Obstructive shock - obstruction of blood flow 3. Distributive shock - abnormal redistribution of blood that result from extensive vasodilation and loss of vascular tone a. Neurogenic b. Cardiogenic - heart unable to maintain adequate cardiac output due to myocardial damage (failure of the heart to pump) c. Septic - has to due with inflammation d. Anaphylactic - has to do with inflammation Symptoms of shock include: increase respiratory rate, high lactate or procalcitonin levels, low o2 sat, high heart rate, low BP, signs of tissue hypoperfusion (cold, clammy skin and cyanosis) Diagnosis can includes CBC, can give clue on cause of shock, lactic acid gives idea on extent of anaerobic metabolism and electrolytes can tell if patient is experiencing end organ damage Mean arterial pressure Stage 1 Stage 2 Stage 3 Early, reversible, compensated shock Intermediate or progressive shock Refractory or irreversible shock Increases heart rate and constriction of blood vessels Activation of renin angiotensin aldosterone system Due to response of kidneys to poor perfusion Strong change of recovery with proper treatment Failure of compensatory mechanisms Decrease in perfusion, leads to cellular hypoxia Neurogenic changes Confusion, disorientation Angina from decrease o2 delivery to myocardium Muscular pain Reversible with proper treatment Declining heart function Shutdown of kidneys Injury to cells in organs and tissues throughout the body Death due to multiple organ dysfunction Hemorrhagic/ hypovolemic shock Loss of more than 15% of body fluids Etiology: hemorrhage, dehydration/diuresis, severe burns Manifestations: rapid breathing, shortness of breath, tachycardia, loss of consciousness, weak pulse, sweating, pale skin, cold hands/feet, urinating less than normal/ none Treatment include maximize o2, prevent further fluid loss, replace fluid lost, basic life support, airway maintenance, supplemental o2, Cardiogenic shock Obstructive shock Heart unable to circle adequate amount of blood Rare condition of obstruction of blood flow to body's organs Diagnosed when acute circulatory failure occurs Etiology: loss of myocardial function and contractility , elevation of diastolic filling pressures and volumes, persistent hypotension, severe reduction in cardiac index Causes include myocardial infarction, heart failure, cardiac tamponade, restrictive cardiomyopathy, and constrictive pericarditis Clinical manifestation: cyanosis with cool skin and mottled extremities, rapid and faint peripheral pulses, low pulse pressure, tachycardia, low and distant heart sounds, peripheral edema and jugular distension, crackles in lungs Diagnosis: first step is diagnose case Treatment: patent airway maintenance, fluid resuscitation (unless pulmonary edema, coronary artery revascularization, correction of acid bad and electrolyte imbalances, intra aortic balloon pump, surgical interventions, pacemakers and defibrillators Pharmacologic therapy: inotropic agents, coronary vasodilators, diuretic, thrombolytics Causes: pulmonary embolism, cardiac tamponade, tension pneumothorax Manifestations: disturbances of consciousness, oliguria, hypotension, tachycardia, decreases cardiac function and circulatory failure Treatment: pneumothorax: dreaces chest tension or pressure on heart, needle thoracostomy and pericardiocentesis for pericardial effusion or cardiac tamponade Pulmonary emboli: surgical removal of block, thrombolytic agent Distributed shock Impaired distribution of blood flow due to extensive vasodilation and loss of vascular tone Etiology: anaphylaxis, adrenal insufficiency, drug reactions, hepatic insufficiency, systemic inflammatory response syndrome — Anaphylactic shock Acute and severe allergic reaction Etiology and pathogenesis includes: antibody Ige, histamine and other substances of anaphylaxis, increased permeability and bronchoconstriction Triggers can be drugs, food, proteins, animal or insect venoms, latex, heavy metal poisoning, exercise and exposure to cold temperature Clinical manifestation include stridor, tachycardia, dyspnea, wheezing, coughing, edema, laryngospasm, bronchoconstriction, angioedema, urticaria, pruritus, hives gastrointestinal cramps, hypotension Treatment includes epinephrine, patent airway, beta agonists, intravenous fluid expanders, vasopressors Diagnosis shock, respiratory symptoms, possible manifestation of anaphylaxis —-Septic shock Organ dysfunction caused by dysregulated host response to infection Immunological, cellular, cardiovascular, hematological systems overwhelmed Sequential Organ Failure Assessment (SOFA) Respiratory, coagulation, hepatic, cardiovascular, neurologic, renal Treatment includes perfusion restored with intravenous fluids, vasopressors, O2 support, broad spectrum antibiotics, infection source control In clue hourly monitoring of o2 sat, pressures of veins/arteries, pulse oximetry, arterial blood gasses, blood glucose, lactate, electrolytes, renal function —Neurogenic shock Caused by blockage of sympathetic nervous system outflow to intrathoracic sympathetic chain Risk factors are spinal cord injuries above T6, brain injury, barbiturate overdose, hypoglycemia, medication, severe pain, spinal anesthesia, vasomotor center depression Clinical manifestation include systolic hypotension, bradycardia, hypothermia, vascular dilation, hypoperfusion of organs, flaccid paralysis below level of injury, priapism Treatment includes fluid replenishment, vasopressors, stabilization of spine and neck, airway patent, oxygen therapy, corticosteroids, atropine Multiple organ dysfunction is the progressive organ dysfunction of two or more systems Risk factors include infection, inflammation, acute lung injury, burn, multiple trauma, ischemia, intoxication, iatrogenic factors, idiopathic factors Six primary systems Respiratory Renal Hepatic Cardiovascular Gastrointestinal Neurogenic Treatment includes optimization of hemodynamic, metabolic, immunologic function, minimizing of iatrogenic injury, fluid resuscitation using volume expanders, inotropic agents, vasoactive agents, mechanical ventilation, protein rich nutrition, targeted antibiotics CHAPTER 27: DISORDERS OF CIRCULATION WITHIN THE CNS CNS made up of brian and spinal cord Detect, transmit, analyze sensory information Generate signals to autonomic and motor pathways that orchestrate visceral and endocrine function, coordination, movement Tissue of CNS rely heavily on receiving constant perfusion for cerebral autoregulation and blood brain barrier Vascular supply is within cranium Internal carotid arteries branch to form anterior and middle cerebral arteries Vertebral arteries join to form basilar artery ○ Internal carotids and basilar artery join to form circle of willis at base of brain Posterior cerebral arteries Two bridging arteries, anterior and posterior communicating arteries Venous drainage of brain travels through bridging veins on brain surface into sinuses: superior sagittal, great cerebral vein of galen, dural venous sinuses and empty into internal jugular vein Disorder of circulation revolve around lack of oxygen and increase pressure in skull Ischemia: obstructed blood vessels or drop in blood flow Pressure: hematoma, excessive production of cerebrospinal fluid blockage of duct system conveying cerebral spinal fluid Production of fluid in choroid plexus of ventricles flowing through ventricular system and subarachnoid space Reabsorbed into venous dural sinuses via arachnoid villi Hydrocephalus is the excessive accumulation of CSF in cranial vault and compresses the surrounding structures, can be caused by lesions that obstruct flow of csF or problems with resorption Blood brain barrier is a specialized endothelium present in brain capillaries Permits selective entry of substances through Tight junctions between endothelial cells Few pinocytic vesicles No fenestra Active transport Substances that cross barrier Highly lipophilic substance cross directly Water crosses membrane by simple diffusion Most nutrients cross barrier by facilitated diffusion Brain receives 15% of cardiac output and consumes 20% of body’s oxygen consumption Cerebral blood flow Autoregulation Blood viscosity Cerebral perfusion pressure Transient Ischemic Attack Ischemic and Hemorrhagic Stroke Temporary episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction Interruption in blood supply to Bleeding from bridging veins region of brain or bleeding of between dura mater and vessels resulting to brain arachnoid membrane tissue damage or infraction Etiology and pathogenesis Ischemica 87% Trauma from high speed Hemorrhagic 13% impact to skull Spontaneous Etiology and pathogenesis Acute subdural hematoma - bleeding Parietal or complete occlusion of cerebral identified after an injury blood flow due to Chronic subdural thrombus or embolus hematoma - brain atrophy Atherosclerosis Clinical manifestations Cardiac disorders Thrombotic strokes Headache, dizziness ○ Internal Confusion, changes in carotid artery behavior ○ Middle Nauseous, vomiting Etiology and pathogenesis Same as ischemic stroke Clot blocking blood supply to region of brain Atherosclerosis Clinical manifestations Facial drooping Subdural hematoma Spinal Cord hemorrhage Rare Etiology and pathogenesis: trauma, vascular malformation, bleeding disorders epidural , subdural, subarachnoid, or intramedullary Clinical manifestations: Sudden, severe back pain with or without radiculopathy Headache Neck stiffness Photosensitivity Irreversible sensory loss below level of Arm of leg weakness on one side of body Speech difficulty Sudden trouble seeing in one or both eyes Difficulty walking with dizziness Lack of balance or coordination Severe headache Modifiable factors include cardiovascular disease, carotid artery disease, diabetes, excess weight, high blood pressure, high cholesterol, cigarette smoking, heavy drinking, physical inactivity, poor nutrition, birth control pills Controversy on hospitalization, but ALL patients should receive urgent evaluation, risk stratification, stroke prevention therapy cerebral artery ○ Basilar artery Clinical manifestation Sudden onset of focal neurologic deficit persisting for at least 24 hours due to reduction or occlusion of cerebral circulation or rupture of blood vessels Others depends on area of brain or spinal cord affecting Treatment Restoration of blood flow and reducing area of infraction ○ Penumbra tissue surrounding infraction Supplemental oxygen Glycemic control Fibrinolytic therapy Antihypertensive therapy Aspirin 325 mg Lethargy or excessive drowsiness, weakness Apathy Seizures Treatment is surgery bleed Treatment Spinal subdural hemorrhage surgical decompression Spinal subarachnoid hemorrhage Surgical resection Catheter based intervention techniques Docarl radiation therapy with gamma knife, cold photon knife FAST - face drooping, arm weakness, speech difficulty, time is crucial 0 = no stroke symptoms 1-4 minor stroke 5 -15 moderate stroke 16-20 moderate to sever 21-42 severe DIABETE MELLITUS General term to group disorders that affect ability to produce or respond to insulin- impaired and affects the body's ability to use energy in food Is the seventh leading cause of death in US Treatment is high priority goals among public health initiatives General symptoms, polydipsia, polyphagia, polyuria, weight loss, nocturia, glucosuria, hypotension, tachycardia, fatigue Type 1 DM (T1D) Type 2 DM (T2D) Almost complete lack of insulin secretion Most common form - t cell mediated autoimmune destruction of pancreatic beta cell Pancreas unable to make Relative insulin deficiency Insulin secretion too low in relation to blood glucose level Insulin resistance and defects in insulin secretion Endogenous insulin unable to produce biological response Destruction of pancreatic beta cells Insulin deficiency considered total or absolute Autoimmune condition Pharmacologic insulin therapy needed for survival Etiology: genetics (HLA genes), family predisposition, environment No dependent on exogenous insulin to sustain like - may need insulin therapy or other medications Most common forms of DM Etiology: genetics, if both parents have risk is 75%, ethnicity (minorities), obesity, high calorie diets, reduces physical activity Eating disorders Diagnosis in nonpregnant adult A1C > or equal to 6.5% Symptoms of diabetes plus casual plasma glucose concentration above or equal to 200 mg/dL Fasting glucose plasma glucose greater or equal to 126 mg/dL 2 hour plasma glucose greater than or equal to 200 mg/dL during an oral glucose tolerance test Pre Diabetes increases risk of developing DM, primary T2D Impaired fasting glucose Fasting blood glucose level or hemoglobin A1C HIGHER than normal but not diagnostic of DM Impaired glucose tolerance Blood glucose level two hours after oral glucose load HIGHER than normal but not diagnostic of DM Requires dietary modification, weight loss, physical activity Labs Hemoglobin A1C Glucose Memory sugar Reflects average blood glucose level for the past 2-3 months Normal - blow 5.7% Prediabetes - 5.7 - 6.4% Diabetes 6.5% Fasting blood sugar level 99 mg/dL or lower = normal 100-125 mg/dL = prediabetes 126 mg/dL or higher = diabetes Non fasting levels are not diagnostic *above 200 warrants + screening Insulin involves the synthesis of glycogen and protein in liver and muscle, triglycerides in adipose tissue and muscle Glycolysis and glucose transport into insulin sensitive tissues Hyperglycemia Hypoglycemia High blood glucose Acuter symptoms increased thirst and urination Weight loss In combo w/ absolute or relative insulin deficiency → acute metabolic emergencies Decreased blood glucose levels primary intention and < secondary Hypoxia delays or stops wound healing process with greatest at center or wound and can lead to wound infection (infection amplifies it) It inhibits fibroblast activity, collagen deposition in matric Stimulus for angiogenesis Reepithelialization occurs only when wound covered with granulation tissue Badly contaminated wounds may overwhelm host defenses and can be largely caused by inappropriate surgical wound handling such as inappropriate suture material increases likelihood of body reaction, break in asepsis, duration of surgery or open time, spill of intestinal contents into peritoneum, failure to proper prepare skin preoperatively Nutrition plays a major role in wound healing especially carbohydrates and fats Malnutrition decreases immune and inflammatory responses, delays wound healing, increases wound infection, diminished angiogenesis, reduces matrix formation and remodeling Vitamins and mineral deficiencies are associated with chronic, nonhealing wounds in nutritionally debilitated individuals Medications can also affects wound healing Corticosteroids promote breakdown of carbohydrates, fats, and proteins and anti inflammatory action impedes inflammatory phase wound healing Antineoplastic drugs are potent immunosuppressants that impair reepithelialization, granulation tissue formation, angiogenesis Abnormal wound healing - deficient, is insufficient deposition of dermal connective tissue matrix weakens tissue to wound failure Clinical manifestations include signs of infection, absence of healing ridge by fifth to ninth postoperative day, seroma or hematoma formation, increase in serous discharge Chronic non healing wound do not processed through healing process or does but cannot maintain structural and functional integrity characterized by an arrest in the inflammatory phase Can harbor bacteria, imbalance between neutrophilic proteolytic enzymes and their inhibitors, increases levels of inflammatory mediators, chronic inflammation, necrosis, fibrosis Pressure injuries are localized ischemic lesions of skin and underlying tissue most commonly over bony prominences because external pressure impair flow of blood and lymph Causes can be immobility, reactive hyperemia, microthrombi, shearing forces Risk factors as immobility or inactivity, poor perfusion, and skin status Clinical manifestations include pressure decreases from boney area toward periphery, discoloration to blisters or areas of denuded superficial skin to deep tissue damage with necrosis, graded or staged to classify degree of tissue damage Treatment is surgical debridement, autolytic debridement, skin grafting, topical and systemic antibiotics, hydrocolloid and transparent film dressing, alginate, foam, iodine dressing RESTRICTIVE PULMONARY DISORDERS Aspiration is entry of secretion of foreign material into the trachea and lung Signs and symptoms depend on the degree of the airway obstruction but include coughing, audible wheezing, and choking Silent aspiration in older adults usually happens because there esophageal muscles don't work properly ○ Mechanisms associated include central or local weakness/ incoordination of the pharyngeal musculature, reduce laryngopharyngeal sensation, impaired ability to produce a reflexive cough, nad low substance P or dopamine levels ○ Symptoms can be silent o overt, usually no symptoms after eating, drinking, vomiting, ot episode of heartburn Secondary pneumonia - aspiration is inhalation of gastric juices or hydrocarbons that trigger inflammatory chance and inactivates surfactant over a large area causing alveolar collapse Acidic gastric juices may damage the airway and alveoli as well as particles contained aspirated gastric juices may obstruct the airways and reduce airflow and lead to another secondary bacterial pneumonia Atelectasis is a complete or partial collapse of the entire lung or lob of the lung occurring when alveoli within the lungs become deflated or possibly filled with alveolar fluid and is the most common breathing complication after surgery There can be no obvious symptoms but some include trouble breathing, cough, and low grade fever Complications include acute pneumonia, bronchiectasis, hypoxemia and respiratory failure, sepsis, pleural effusion and empyema Treatment Surgical Non surgical Lobectomy Chest physiotherapy Bronchoscopy Breathing exercises Drainage Obstructive atelectasis Non Obstructive atelectasis Happens when a blockage develops in one of the airways Inhalation of a foreign object in an airway Mucus plug (buildup) in an airway Tumor growing within an airway Tumors in the lung tissue that presses on the airway Refers to any type of atelectasis that isn’t caused by some kind of blockage in the airways Surgery Pleural effusion Pneumothorax Lung scaring Surfactant deficiency Purpose of incentive perimeter is Increase transpulmonary pressure and inspiratory volumes Improve inspiratory muscle performance Reestablish or stimulate the normal pattern of pulmonary hyperinflation Pulmonary sarcoidosis is an inflammatory disease that affects multiple organs in the body, but mostly the lungs and lymph nodes and can lead to scar tissue in your lungs while also making them function more poorly Characterized by abnormal masses or nodules called granulomas consisting of inflamed tissues forming in the lungs Pneumothorax is when air enter space between the visceral pleura and the parietal pleura and that excess air places extra pressure on the lung inside the cavity and making the lung unable to expand for appropriate gas exchange Oxygen decreases and co2 increases Treatment is to reestablish negative pressure in the pleural cavity and allow for drainage or air or fluids Pleural effusion is the collection of excess fluid in the pleural space to which common causes are pneumonia, TB, pulmonary effusion, malignant disease, cardiac failure, subdiaphragmatic disorders Treatment is thoracentesis to remove fluid (reduces symptoms) and also find the cause Chest wall abnormalities Flail chest which is a life threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall, causes chest pain and SOB Deformities include pectus excavatum - sinken or funnel chest and pectus carinatum - pigeon chest Kyohoscoliosis Paradoxical breathing Acute respiratory distress syndrome (ARDS) results from a massive inflammatory response with acuter, diffuse, severe alveolar capillary wall damage that result in progressive noncardiogenic pulmonary edema and respiratory failure Considered restrictive due to the increase alveolar pressure that develops which causes the alveoli to collapse during expiration Empyema is the collection of pus in the pleural space occurring as a complication of pneumonia, but can occur after a thoracentesis, lung surgery, with a lung abscess, or following chest trauma Intercostal retraction are mvmts that occur due to reduces air pressure inside chest, trachea or bronchioles become partially blocked and the intercostal muscles are sucked inward, between ribs during breathing Idiopathic pulmonary fibrosis is a disease the results in scarring, fibrosis, of the lungs for an unknown reason which worsen overtime and become hard to take in a deep breath and the lungs cannot take in enough oxygen Symptoms include gradual onset of SOF and a dry cough Treatment includes medications, oxygen therapy, nonmedical treatments such as exercise, lung transplant OBSTRUCTIVE PULMONARY DISEASES *hemoptysis is blood in sputum * primary etiology of all is inflammation Chronic bronchitis is cases by inspired irritants that increase mucus production and the size and number of mucus glads → inflammation Extension of inflammatory changes to alveoli Loss of mucociliary function Replacement of ciliated epithelium with squamous cells Decreased action of cilia present Mucus plugs, thicker than usual —> narrow airways Emphysema is an abnormal permanent enlargement of the gas exchange airways accompanied by destruction of alveolar walls Blebs are small subpleural thin walled air containing spaces no larger than 1 to 2 cm in diameter with walls less than 1 mm thick If they rupture, they allow air to escape into pleural space resulting in a spontaneous pneumothorax Bronchitis vs emphysema Bronchiectasis is the permanent enlargement of parts of the airways of the lungs with symptoms being chronic cough, productive with mucus Can be due to an infection or another condition, sometimes not known People are risk are those with cystic fibrosis, immunodeficiency disorders, disorder that affect ciliary function Can develop at any age, more common in women (⅔) Cystic fibrosis is a progressive genetic disease that causes persistent lung infections that limit the ability to breath over time caused by a defective gene that causes a thick, sticky buildup of mucus in the lunge, pancreas, and other organs Recessive disease In the lungs, the mucus clogs the airways and traps bacteria leading to infections, extensive lung damage, and eventually respiratory failure Pulmonary symptoms include persistent coughing, sometimes with phlegm, frequent lung infections including pneumonia or bronchitis, and wheezing or SOB Treatment is airway clearance techniques that loosed thick sticky mucus so it can be cleared from the lungs by coughing or huffing and this can decrease lung infections and improve function Medications include antibiotics, mucus thinners, and nebulizer treatments with bronchodilators CFTR modulator therapy, CFTR protein regulates the proper flow of water and chloride in and out of cells lining the lungs and other organs In people with CF, mutations in the CFTR gene result in either a defective protein being produces or no protein at all b/c different mutations cause different defects in the proteins, teh medications that have been developed so far are effective only in people with specific mutations A newer treatment is trikafta approved for patients 12 years and older who have a least one f508del mutation in the cystic fibrosis transmembrane conductance regulator gene which is estimated to represent 905 of the cystic fibrosis population Atopy is a syndrome characterized by a tendency to ber hyperallergic and usually present as eczema, allergic rhinitis (hay fever), and allergic asthma Asthma is an inflammatory disorder of the airways, acute of chronic characterized by bronchial hyperreactivity and reversible airflow obstruction usually in response to an allergen resulting from a complex interaction between genetic susceptibility, environmental factors, and infections, usually viral Mast cells are activated by irritants and or igE (trigger) Inflammation → hyper responsiveness Obstruction occurs secondary to bronchoconstriction, mucus plugs, inflammation Inflammatory mediators cause: bronchial SM spasm, airways edema, vascular congestion and increased capillary permeability, mucus increases, impaired ciliary function, second wave mediators obstruction, pulmonary remodeling Atopic dermatitis NEOPLASTIC AND INFECTIOUS DISORDERS OF THE PULMONARY SYSTEM Influenza is a highly contagious virus the has a short incubation period, influenza with pneumonia is the 8th leading cause of death in the US Pneumonia is an acute infection of the lung parenchyma that commonly impairs gas exchange Classification can be done by origin (viral, bacterial, fungal, protozoal), location (bronchopneumonia (distal airways and alveoli) o lobar (either part of a lob or all), and type (primary or secondary) Risk factors include chronic illness and debilitation, cancer (primarily lung), abdominal and thoracic surgery, atelectasis, cold of viral respiratory infections, chronic respiratory disease like COPS, bronchiectasis, cystic fibrosis Bacterial pneumonia Viral pneumonia Hospital acquired pneumonia (HAP) Healthcare associated pneumonia (HCAP) Ventilator associated pneumonia Can occur in any part of the lung Trigger alveolar inflammation and edema Produces an area of low ventilation with normal perfusion Capillaries become engorged with blood Virus first attacks bronchiolar epithelial cells and also invades bronchial mucus glands and goblet cells then spread to alveoli Fills with blood and fluid Lower respiratory infection that was not incubating at the time of hospital admission and that presents clinically 2 or more days after hospitalization Pneumonia in nonhospitalized patients who had significant experience with the healthcare system Such contact could include 1) intravenous therapy for wound care within the preceding 30 days 2) residence in a long-term care facility Forma od nosocomial pneumonia that occurs in about 22.8 patients patients receiving mechanical ventilation for longer than 48 hours Associated with increases in morbidity and mortality, hospital length stay, and costs The mortality rate attributable to VAP is 3) hospitalization in an acute-care hospital within the preceding 90 days, and/or 4) outpatient treatment in a hospital or hemodialysis clinic within the preceding 30 days 27% and has been as high as 43$ when the causative agent was antibiotic resistant Cigarette smoking is responsible for 85 - 90% of lung cancers, cigarette smoker are 15 times more likely to die that lifelong non smokers, when comparing by gender, male smoker have a 23 fold increase in likelihood to develop while female smoker are 13 times more likely to develop Small cell lung cancer (oat cell cancer) Non small cell cancer Most aggressive form of lung cancer that usually starts in the bronchi and grow very quickly creating large tumors and also metastasize quickly Majority of lung cancers (85 - 90%) comprised of three primary subtypes Adenocarcinoma Squamous cell carcinoma Large cell carcinoma *further classified as well differentiated or not Accounts for 10-15% of lung cancer Symptoms of lung cancer include: persistent cough with or without production(common), sputum streaked with blood, obstructive pneumonia, dyspnea, chest pain, hoarseness if recurrent laryngeal nerve is compressed/invaded by tumor, paraneoplastic syndromes with advanced lung cancer In the US TB transmission primarily between infected person and susceptible person by inhalation of aerosolized droplets contaminated with mycobacterium TB About 3-4% of ppl with primary TB infection develop disease during first year after exposure and then up to 15% after first year Active stage - air bone precautions, latent stage - can become active if immune system is compromised, exposed - positive PPD without signs of disease Symptoms include: cough, weight loss and anorexia, fever, night sweats, dull aching chest pain, hemoptysis, 20% are asymptomatic Diagnosis of active TB includes chest x ray, sputum culture for acid fast bacteria, quanti feron gold assay Bacilli calmette guerin BCG, is vaccine for TB and many foreign born person have been BCG vaccinated, especially in countries with high prevalence of TB to prevent childhood TB meningitis Core of each treatment regimen is a combination of four medications: isoniazid, rifampin, pyrazinamide, ethambutol Initial 2 month treatment phase is followed by a continuation treatment phase of 4 to 7 months Valley fever is a fungal lung infections characterized by fever, cough, chest pain, chills, night sweats, headache, fatigue, joint aches, red spotty rashes Diagnosis required sputum culture for presence of coccidioides organisms and blood tests checking for antibodies against the fungus that causes valley fever Treatment is antifungals Oral for serious and IV for life threatening A single bout of valley fever results in lifelong immunity, but relapse is possible, especially if the body's immune system become significantly weakened (same for TB) If progresses can become chronic from of pneumonia most common in ppl with weakened immune system characterized by low grade fever, weight loss, cough, chest pain, blood tinged sputum, nodules in lungs Pulmonary embolism is the occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, and or air bubbles commonly arising femur the deep vein in the thigh Virchow traid? Disorder of the upper respiratory tract - children Croup is acute laryngotracheobronchitis common in children 6 months to 5 years caused by a virus (parainfluenza, influenza a or RSV) and causes subglottic edema Usually occurs after an episode of rhinorrhea, sore throat, low grade fever, inspiratory stridor, hoarse voice Causes a seal like barking cough Usually resolves within 24 to 48 hours but severe cases are treated with nebulized epinephrine Acute epiglottitis is a server rapid progressive life threatening infection of the epiglottis and that surrounding areas historically caused by haemophilus influenzae type B but 80-90% decreased incidence due to the HIB vaccine Symptoms include: high fever, irritability, sore throat, inspiratory stridor, muffled voice, severe respiratory distress Treatment is emergency airway and antibiotics/steroids The epiglottis is a flap made of elastic cartilage covered with mucous membrane attached to the entrance of the larynx that stands open during breathing, allowing air into the larynx but during swallowing it closes to prevent aspiration forcing the liquids or food to go down the esophagus instead - Controls if something goes into the trachea or esophagus Disorder of lower respiratory tract - children Pneumonia in children primary cause is viral usually in kids less than 3 weeks to 4 years as younger children are unable to increase cardiac stroke volume to increase oxygenation to tissues First signs in children will be tachypnea Bronchitis is most commonly caused by the pathogen respiratory syncytial virus RSV, and is the major reason for hospitalization of infants and younger children Manifestations include rhinorrhea, tigh cough, decreased appetite, lethargy, fever, wheezing Pertussis whooping cough is a highly contagious respiratory infection that is usually caused by bordetella pertussis directly transmitted by inhalation of contaminated droplet or indirectly by touching fomites contaminated by secretion for a person in the acute stage of the illness This pathogen attaches to and damaged ciliated respiratory epithelium Symptoms include uncontrollable spasmodic cough that end in a loud crowing inspiratory whoop, cough may be so hard it induces vomit Myalgias, fever also common As progresses, sputum become more tenacious, pneumonia become a common complication Infection lasts about 6 weeks but cough can persist for 3 to 4 months Cardiac disorders Heart failure is the inability of the heart to pump adequate amount of blood to meet the body’s metabolic needs Can happened in as a result of different reasons Volume overload and fatigue - muscle relaxation: heart does not fill adequately Decreases cardiac output - muscle contractions: decrease ejection of blood out of heart General symptoms are SOB, swelling of the extremities, fatigue Causes include disorder of heart muscle, pericardium and heart valves, restricted blood supply to heart, and abnormalities of blood vessels leading out of heart Cardiac output is the amount of blood pumped from the left and right ventricle in one minute CO=SV×HR Stroke volume (SV) : the amount of blood pumped from the ventricle during one contraction Preload: volume in the right or left ventricle at the end of diastole (ventricular filling) Afterload: force that the heart has to contract against to eject blood from the ventricle during systole (contraction/ejection) Ejection fraction is the measurement of the percentage of blood ejected from the left ventricle with each contraction, normale is 55% or higher Heart issues are a progressive disorder with compensatory mechanisms, secondary damage and cardiac decomposition. In additional there is an activation of RAAS systems and compensatory mechanisms can become maladaptive Acute Chronic (decompensated) Heart Failure Chronic Heart Failure Worsening symptoms, hospitalization required More common and requires long term management, because it is progressive Many causes: stress, infection, diet and nonadherence, poor health status decision making, high BP, myocardial ischemia, alcohol consumption Staging heart failure is in collaboration with the American college of cardiology and AHA, four stages Killip classification is based on severity of HF symptoms due to depression of heart muscle function - confirmed coronary syndrome- used for mortality prediction Left sided heart failure Right sided heart failure Left side of heart is unable to pump blood sufficient to meet needs of body Right side of heart is unable to pump blood to meet needs of body Caused include: cardiomyopathy, coronary artery disease, alcohol or cocaine abuse, hypertension Causes include: left sided HF, pulmonary embolism, sickle cell crisis, stenosis of pulmonary or mitral valve, pulmonary hypertension, ischemia or myocardial infarction Clinical manifestations include : decrease BP, orthopnea, cough, cracked, rales, heart murmurs or gallops, pulmonary edema, fatigue, exercise intolerance Diagnosis includes echocardiogram, pulmonary artery catheterization, lab exams Treatment include diuretics, aCE inhibitors or ARBs, beta blockers, aldosterone antagonist, self care activities, management of associated disorders Fluid back up to lungs Clinical manifestation include: elevated jugular venous pressure, distended neck veins, cool extremities, poor distal pulses, fatigue, exercise intolerance, syncope, nausea or vomiting, abdominal pain and or lack of appetite, peripheral edema, ascites, hepatomegaly Diagnosis include transthoracic echocardiology and pulmonary artery catheterization Treatment includes: treatment of LVHF, low sodium diet, diuretics, direct acting pulmonary vasodilators, intravenous inotropes, surgical treatment similar to left sided Replacement of pulmonary or mitral valves Right ventricular assist device placement Cardiac transplantation Fluid back up to body Systolic heart failure Diastolic heart failure Impaired contraction of heart muscle with reduced ejection Cam not fill with blood during relaxation period Normal contractility but abnormal relaxation of heart Decrease CO and BP Causes include dilated cardiomyopathy, coronary artery disease with myocardial infarction, metabolic causes, pregnancy Etiology and pathogenesis Stiffness of heart muscle cells or proteins and connective tissues Abnormal electrolyte movement No direct cause; linked to other disorders Manifestation include fatigue, sleep disturbances, weight loss, anorexia, dyspnea, depression and cognitive dysfunction Diagnosis includes Transthoracic echocardiography, X-ray Treatment: Pharmacological therapies Angiotensin-converting enzyme (ACE) inhibitors Angiotensin receptor blockers (ARBs) Clinical Manifestations Renal insufficiency Fluid retention, especially abdomen Pulmonary and hepatic congestion Dyspnea Diagnosis & Treatment Symptoms of HF without reduced EF Cautious use of diuretics Beta blockers Vasodilators Diuretics New medical therapies Treatment of underlying disease ACE inhibitors and beta blockers ineffective Self-care activities, education: Low sodium diet, implantable cardioverter-defibrillator, implantable biventricular pacemaker, left ventricular assist devices (LVADs) High output heart failure means CO greater than 8 L/min Etiology and pathogenesis Unusually low SVR and elevated CO Dilation of vascular bed Arteriovenous fistulas: abnormal connection between an artery and a vein Clinical Manifestations: warm extremities + strong distal pulses, hepatic congestion, elevated jugular venous pressure, peripheral edema, fatigue, dyspnea Treatment: treatment of underlying cause of vasodilation, control of symptoms, support of vital functions, beta-blocker therapy, controlling shunt between arterial and venous beds, supportive care VASCULAR DISORDERS Tissues depends on vascular system for survival and lack of sufficient blood flow can lead to hypoxia and a buildup up waste products Central perfusion Local perfusion Blood flow pumped by heart to entire vascular system Cardiac output and blood pressure Pathologic processes affect entire body Volume of blood flowing through specific tissue Controlled by capillaries serving region Pathologic processes affect specific tissues Peripheral vascular disease refers to conditions affecting circulation is tissues other than the brain or heart Includes peripheral artery disease and diseases affecting the veins Risk factors include: SMOKING, hypotension, coronary artery disease, high cholesterol, diabetes, family history of vascular disease, Obesity, sedentary life, men more often than women, adults over 50 Aterial - dry Venous - wet Varicose veins are a result of weakened valves and veins, usually in the dependent areas such as legs, ankles, and feet The one way valves in veins keep blood from flowing from the legs up towards the heats and veins can become weak, large, and twisted Risk factors include lifestyle (job with long standing hours), genetics, pregnancy, aging, obesity Treatment: PREVENTION is key - elevating legs, changing positions frequently, compression socks Weight loss, exercise, sclerotherapy, laser Venous thrombosis or DVT occurs when blood clots form in veins located deep inside the body and can cause leg swelling or pain but can also be asymptomatic. It can be caused by anything that prevents the blood from circulating or clotting normally, injury, surgery, limited movement (prevention is also key) Risk factors include inheriting blood clotting disorder, prolonged best rest or sitting, injury or surgery, pregnancy, birth control pills, hormone replacement therapy, smoking Diagnosis usually requires D dimer test and ultrasound Embolism is the lodging of a blockage incuse a blood vessel, usually a thrombus but can also be fat globule, bubbles of air, gas embolism, or a foreign material Pulmonary Embolism: occurs when a blood vessel in your lung becomes blocked by a blood clot (thrombus) that travels to your lung fro Arteriosclerosis is the thickening and loss of elasticity of arterial wall because of calcification Atherosclerosis is a type caused by plaque buildup Risk factors include SMOKING, hypertension and heart disease, high levels of cholesterols, high levels of LDLs, diabetes and or obestory, advanced age, physical inactivity Major clinical manifestation include MI, stoke, PAD Treatment involves lifestyle changes, medications, and surgery to open occluded arteries (angioplasty, stent) Nonatherosclerotic peripheral arterial disease (NAPAD) is a group of disorders in which blood flow is decreased for reasons other than plaque buildup for example raynaud's disease with causes decreased blood flow to the fingers because of spasms of blood in those areas in response to cold, stress, or emotional upset Specifically about raynaud disease, manifestations include pale skin, cyanosis, numbness, tingling, burning sensation, ischemia Treatment include avoiding triggers, anti inflammatory meds, calcium channel blockers Chronic venous insufficiency is when the veins are unable to return adequate blood to the heart with most common causes being deep vein thrombosis and varicose veins Commonly associated with genetic predisposition, pregnancy, age over 50, smoking, lack of physical activity, sanding or sitting for long periods, contraceptives (oral) Clinical manifestation include leg ulcers, varicose veins, DVT Treatment includes preventative measures and education such as exercise, compression socks, smoking cessation, and weight loss as well as radiofrequency, laser ablation, anticoagulants Hypertension is the consistent elevation of blood pressure above 140 mmHg systolic or above 90 mmHg diastolic (can be primary or secondary) Long term consequences include stroke, heart failure, MI, chronic kidney disease, vision loss, headaches, erectile dysfunction, chest pain and dyspnea Treatment include both non pharmacological and pharmacological approaches Some nonpharmacological approaches include restrict sodium consumption, smoking cessation, limit alcohol optimal wight Primary hypertension Secondary hypertension No known cause but he most common, 90% Has an identifiable cause such as hyperthyroidism, chronic kidney disease, tumors of the adrenal land… therefore treatment is to remove and address the underlying cause Associated factors include genetics, age, race, diet, smoking and alcohol consumption sedentary lifestyle Postural hypotension - Orthostatic BP is when there is a fall in Bp of more than or equal to 20 mmHg systolic or more than or equal to 10 mmHg diastolic or both within 3 minutes of standing upright, this increases the risk of falls, syncope, Cv event in elders CORONARY CIRCULATION DISORDERS Coronary artery disease results in a reduced supply of oxygen and nutrients Diagnosis includes presence of dysrhythmia, blood tests, stress test, echocardiography, SPECT Treatment includes lifestyle changes, hypertension management, lipid lowering therapy, anxiety management Myocardial ischemia and infarction is often characterized by atherosclerosis which causes narrowed coronary arteries. Decrease blood flow, fracture in fibrous cap, and superficial erosion of intima. Because of the disruption on coronary blood flow, there is an imbalance among o2 supply, demand, and consumption Stable angina Unstable angina Occurs with increase myocardial oxygen demand and reduced blood flow during exertion or emotional stress Sometimes referred to acute coronary syndrome and causes unexpected chest pain, usually during rest Clinical manifestation are related to exertion and resolve with rest r short acting nitroglycerin Treatment includes risk factor modification, ASA medication, antihypertensives (beta blockers) Does not respond well to low dose nitroglycerin and can lead to MI if not treated quickly The most common cause is reduced blood flow to heat muscles because the coronary arteries are narrowed by atherosclerosis Symptoms are similar to an MI Coronary microvascular disease involves damage to walls and of small coronary arteries with the cause not clearly understood Clinical manifestation includes angina in absence of myocardial ischemia Specific acute coronary syndromes are active form of CAD with three different subtypes Risk factors include CA and other triggers, CAD most commonly progresses to its actual form Non ST segment elevation acute coronary syndrome ST segment elevation myocardial infarction NSTEMI and unstable angina Most precise definition of heart attack Risk factor is smoking Severe chest lasting more than 20 minutes Prevention of death requires recognition reperfusion treatment and management Treatment include supplemental o2, nitroglycerin, morphine sulfate, beta blockers Manifestation includes classic chest pain and dyspnea, malaise and fatigue, radiating pain Treatment is PCI, CABG, antiplatelet therapies, anticoagulation agents, morphine for pain Ventricular aneurysm is a defect in the left or right ventricle ll and it cause bulging outward during systole and diastole, result of MI Treatment is aneurysmectomy and management of complications Pericarditis and dressler syndrome is the swelling and inflammation of pericardium that results from injury Occurs 2-3 weeks after MO with unknown pathogenesis, autoimmune with manifestations including chest pain worsening with deep inspiration, coughing, swallowing, or lying in supine position Treatment includes hospitalization for management and observation of possible cardiac tamponade, aspirin Cardiac tamponade involves increased pericardial pressure b/c blood or fluid buildup between myocardium and pericardium Pulse paradox is an abnormally large decrease in stroke volume systolic blood pressure and pulse wave amplitude during inspiration, a normal fall in pressure is less than 10mmHg (checked with apical heart beat while feeling radial pulse) Valvular disorders involves disruption of blood flow through atria and ventricles Stenosis - narrowing of the valvular orifice that prevents adequate outflow of blood Regurgitation - leaflets fail to close correctly and are unable to prevent backflow of blood Risk factors are older age, femal, large infarct size, heart failure, history of ACS or CAD When is it mild or moderate there are no symptoms but when acute severe it can lead to SOB, fatigue, murmurs, pulmonary edema, shock Treatment involves surgery, treatment of coexisting disease, diuretics, vasodilators, Mitral regurgitation is when the mitral valve doesn’t shut all the way and blood can leak back into the left atrium Mitral valve prolapse is a condition in which the two valve flaps of the mitral valve does not close smoothly of evenly and instead bulges upward into the left atrium Pts may not experience symptoms unless servers and stroke is a risk if blood backs up and becomes static, clots can form Mitral valve stenosis is the narrowing of the heart's mitral valve, does not open properly and bocks flow into the left ventricle Symptoms progress slowly over time - SOB especially with exertion or lying down, fatigue especially during exercise, swollen legs or feet, palpitation, dizziness/ fainting Aortic stenosis is related to the aortic valve of the heart which controls blood flow to the rest of the body and a critical component of successful blood flow is the ability of the aortic valve to open wide and close tight. It is often calcium buildup that causes the shrinkage Aortic regurgitation occurs when the aortic valve does not close tightly and allows some of the blood that was pumped out of the left ventricle to leak back into it, can prevent the heart form efficiently pumping blood to the rest of the body Hyperlipidemia -overall high cholesterol, Hypercholesterolemia - high ldl Heart attack (blockage and ischemia) is not cardiac arrest (heart just stops) NOT THE SAME