AH1 EXAM 2

Answer: D Rationale: Anemia in the older adult population is commonly caused by co-morbid conditions such as cancer or renal disease.

At an outpatient clinic, K.L.'s 78-year-old grandma is found to have a Hgbof 8.7 g/dL(87 g/L) and a Hct of 35%. Based on the most common cause of these findings in the older adult, the nurse collects information regarding a.a history of jaundice and black tarry stools. b.a 3-day diet recall of the foods the patient has eaten. c.any drugs that have depressed the function of the bone marrow. d.a history of any chronic diseases such as cancer or renal disease.

Infective Endocarditis (IE)

= *Infection of inner layer of heart, including the cardiac valves* §Improved prognosis with *antibiotic therapy* CAUSES: *Bacterial most common:* §Streptococcus viridans §Staphylococcus aureus Viruses Fungi RISK FACTORS: §Cardiac, noncardiac, procedural Principal risk factors: §Age §IV drug abuse (IVDA) §Prosthetic valves §Use of intravascular devices §Renal dialysis CLINICAL MANIFESTATIONS: §Nonspecific §Fever §Chills §Weakness §Malaise §Fatigue §Anorexia §New or worsening systolic murmur in most patients §Heart failure subacute form: §Arthralgias §Myalgias §Back pain §Abdominal discomfort §Weight loss §Headache §Clubbing of fingers vascular: §Splinter hemorrhages in nail beds §Petechiae §Osler's nodes on fingertips or toes §Janeway's lesions on pads of the fingers and toes §Roth's spots DIAGNOSIS: §History Laboratory tests: §Blood cultures §CBC with differential §ESR, C-reactive protein (CRP) §Echocardiography §Chest x-ray §ECG §Heart catheterization CARE: §Accurate identification of organism §*IV antibiotics (long-term; 4-6 WEEKS)* §Repeat blood cultures §Valve replacement if needed §Antipyretics §Fluids §Rest §Compression stockings §ROM exercises §Deep breath and cough every 2 hours

Heart Failure

= Complex clinical syndrome resulting in insufficient blood supply/oxygen to tissues and organs §Involves diastolic or systolic dysfunction §Ejection fraction (EF) is amount of blood pumped by LV with each heart beat RISK FACTORS: Hypertension: Modifiable risk factor §Properly treated and managed, incidence of HF can be reduced by 50% CAD: Co-morbidities contribute to development of HF ETIOLOGY: §Anything that interferes with mechanisms that regulate cardiac output (CO) §Ventricular failure leads to: §Low blood pressure (BP) §Low CO §Poor renal perfusion Natriuretic peptides: §Atrial natriuretic peptide (ANP),b-type natriuretic peptide (BNP) §Released in response to increased blood volume in heart §Causes diuresis, vasodilation, and lowered BP §Counteracts effects of SNS and RAAS COMPLICATIONS: §Pleural effusion = fluid between 2 layers of membranes. §Dysrhythmias - atrial and ventricular §Left ventricular thrombus §Hepatomegaly §Renal failure DIAGNOSTIC STUDIES: Echocardiogram: §Provides information on EF, heart valves and heart chambers §ECG, chest x-ray, 6-minute walk test, MUGA scan, cardiopulmonary exercise stress test, heart catheterization, EMB §*BNP levels will be increased*.

Aplastic Anemia

= Pancytopenia: •Decrease in all blood cell types •Red blood cells (RBCs) •White blood cells (WBCs) •Platelets •Hypocellular bone marrow •Ranges from chronic to critical : •The spectrum of the anemia can range from a chronic condition managed with erythropoietin or blood transfusions to a critical condition with hemorrhage and sepsis. CAUSES: Rare: •Annual rate of 2-5 new cases/million/year Usually acquired: •Idiopathic •An autoimmune basis is presumed CLINICAL MANIFESTATIONS: •Symptoms caused by suppression of any or all bone marrow elements General manifestations of anemia: •Fatigue, dyspnea •Cardiovascular and cerebral responses •Neutropenia: *infection, high temp.* •Thrombocytopenia is manifested by a predisposition to bleeding evidenced by *petechiae, ecchymosis, and epistaxis.* DIAGNOSTIC STUDIES: laboratory studies confirm diagnosis: •Low Hgb, WBC, and platelet values •Low reticulocyte count •Elevated serum iron and total iron-binding capacity (TIBC) •Hypocellular bone marrow with increased fat content (yellow marrow) *BONE MARROW BIOPSY* CARE: •Identify and remove causative agent (when possible) •Provide supportive care until pancytopenia reverses •Prevent complications from infection •Prevent hemorrhage •Immune therapies and bone marrow transplantation can be curative: hematopoietic stem cell transplant (HSCT) and immunosuppressive therapy with antithymocyte globulin (ATG) and cyclosporine or high-dose cyclophosphamide (Cytoxan).

Answer: B Rationale: Induction is aggressive treatment that seeks to bring about remission by the destruction of leukemic cells. During induction therapy, the bone marrow is severely depressed by the chemotherapy agents, and neutropenia, thrombocytopenia, and anemia may occur. High-dose chemotherapy is administered immediately after the induction phase.

A patient with acute myelogenous leukemia is starting chemotherapy. When teaching the patient about the induction stage of chemotherapy, what is an appropriate statement? a."The drugs are started slowly to minimize side effects." b."You will be at increased risk for bleeding and infection." c."High doses will be administered every day for several months." d."Most patients have more energy and are resistant to infection."

Chronic Stable Angina

Falls under umbrella of CAD •Angina = clinical manifestation: •Occurs when arteries are blocked 70% or more •(50% or more for left main coronary artery) •Intermittent chest pain that occurs over a long period with same pattern of onset, duration, and intensity of symptoms •Few minutes in duration •ST segment depression and/or T-wave inversion •Control with drugs: •*Short-acting nitrates: nitroglycerin* = FIRST LINE Dilate peripheral and coronary blood vessels Give sublingually or by spray If no relief in 5 minutes, call EMS; if some relief ,repeat every 5 minutes for maximum 3 doses. •Long-acting nitrates To reduce angina incidence Main side effects: headache, orthostatic hypotension Methods of administration •Oral •Nitroglycerin (NTG) ointment •Transdermal controlled-release NTG DRUG THERAPY: ANGINA: EF = < 40% ACE ARBS Antiplatelets B-Blockers CCB Nitrates Lipid-lowering drugs DIAGNOSTIC STUDIES: Chest x-ray 12-lead ECG Laboratory studies: C-reactive protein, lipid profile Echocardiogram Exercise stress test EBCT CCTA Cardiac Cath •Alternative therapies for refractory chronic stable angina: *Enhanced external counter pulsation (EECP):* •Inflatable cuffs are placed around legs •Increase venous return •Augment DBP Spinal cord stimulation CARE: "*The treatment of chronic stable angina aims to decrease O2 demand and/or increase O2 supply.* reduction of risk factors

Megoblastic Anemias: Pernicious Anemia

Group of disorders: •Caused by impaired DNA synthesis •Presence of megaloblasts (large, abnormal RBCs) Majority result from deficiency in: •Cobalamin (vitamin B12) •Folic acid COBALAMIN DEFICIENCY: •*Cobalamin deficiency is vitamin B12 deficiency.* *Intrinsic factor (IF):* •Protein secreted by parietal cells of gastric mucosa •If IF is not secreted, cobalamin will not be absorbed CAUSES: Most commonly caused by pernicious anemia: •Which is caused by an absence of IF •Insidious onset •Begins in middle age or later (40-60) •Predominant in Scandinavians and African Americans Can also occur: •GI surgery •Chronic diseases of the GI tract •Excessive alcohol or hot tea ingestion = folic acid •Smoking •Long-term users of H2-histamine receptor blockers and proton pump inhibitors •Strict vegetarians CLINICAL MANIFESTATIONS: General manifestations of anemia develop slowly due to tissue hypoxia GI manifestations: •Sore tongue, anorexia, nausea, vomiting, and abdominal pain *Neuromuscular manifestations:* •*Weakness, paresthesiasof feet and hands,* ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes DIAGNOSTIC STUDIES: •Macrocytic RBCs have abnormal shapes and fragile cell membranes •Serum cobalamin levels are decreased •Normal serum folate levels and low cobalamin levels suggest megaloblastic anemia is due to cobalamin deficiency •Upper GI endoscopy *Schilling Test* = measures vitamin B12 absorption with and without intrinsic factor; used to differentiate between malabsorption and pernicious anemia. CARE: •Parenteral or intranasal administration of cobalamin is the treatment of choice. •Patients will die in 1-3 years without treatment •This anemia can be reversed with ongoing treatment but long-standing neuromuscular complications may not be reversible FOLIC ACID DEFICIENCY: •Also a cause of megaloblastic anemia •Folic acid is required for DNA synthesis •RBC formation and maturation •Clinical manifestations are similar to those of cobalamin deficiency, but absence of neurologic problems differentiates them •GI disturbances include dyspepsia and a smooth, beefy red tongue. CAUSES: •Dietary deficiency •Malabsorption syndromes •Drugs •Increased requirement •Alcohol abuse and anorexia •Loss during hemodialysis DIAGNOSTIC STUDIES: •Serum folate level is low •Normal is 3 to 16 mg/mL (7 to 36 mol/L) •Serum cobalamin level is normal CARE: •Treated by replacement therapy •Usual dose is 1 mg per day by mouth •Encourage patient to eat foods with large amounts of folic acid •Patients with a family history of pernicious anemia should be evaluated for symptoms because there is a familial predisposition for it. •Diminished sensations to heat and pain from neurologic impairment •Regular screening for gastric cancer

Sickle Cell Disease (SCD)

Group of inherited, autosomal recessive disorders: •Characterized by presence of an *abnormal form of Hgb in RBC* •Genetic disorder usually identified during routine neonatal screening •Incurable and often fatal by middle age because of renal failure, infection, pulmonary failure, and/or stroke. CAUSES: •Abnormal hemoglobin, HgbS, causes the RBC to stiffen and elongate •Erythrocytes take on a sickle shape in response to ↓ O2 levels TYPES OF SCD: *Sickle cell anemia:* > Most severe > Homozygous for hemoglobin S (HgbSS) *inherited from both parents.* •Sickle cell thalassemia •Sickle cell HgbC disease •Sickle cell trait (HgbAS) SICKLING EPISODES: •The major pathophysiologic event of this disease: •Triggered by *low O2* tension in blood •*Infection is most common precipitating factor.* Other events that can trigger or sustain a sickling episode include dehydration, increased hydrogen ion concentration (acidosis), increased plasma osmolality, decreased plasma volume, and low body temperature •(Initially, sickling is reversible with re-oxygenation* •vaso-occlusive phenomena and hemolysis are the clinical hallmarks of sickle cell disease. SICKLE CELL CRISIS: •*Severe, painful, acute exacerbation of sickling causes a vaso-occlusive (constriction) crisis* •Severe capillary hypoxia eventually leads to tissue necrosis •Life-threatening shock is a result of severe O2 depletion of the tissues and a reduction of the circulating fluid volume CLINICAL MANIFESTATIONS: SCD •Typical patient is asymptomatic except during sickling episodes Symptoms may include: •*Pain from tissue hypoxia and damage* •Pallor of mucous membranes •Jaundice from hemolysis •Prone to gallstones (cholelithiasis) •Pain episodes are often accompanied by clinical manifestations such as fever, swelling, tenderness, tachypnea, hypertension, nausea, and vomiting. COMPLICATIONS: •*Infection is a major cause of morbidity and mortality* •Infections can be so severe that they can cause an aplastic and hemolytic crisis and gallstones. •Function of spleen becomes compromised from sickled RBCs > Autosplenectomy (spleen becomes small) is a result of scarring •Pneumococcal pneumonia most common •Severe infections can cause aplastic crisis > Can lead to shutdown of RBC production in bone marrow. *Acute chest syndrome:: * •Pulmonary complications that include pneumonia, tissue infarction, and fat embolism •Characterized by fever, chest pain, cough, pulmonary infiltrates, and dyspnea •*Leads to multiple serious complications: renal failure, PE, stroke, osteoporosis, chronic leg ulcers around ankles, priapism (persistent penile erection) if penile veins become occluded.* DIAGNOSTIC STUDIES: •Peripheral blood smear •*Sickling test* •Electrophoresis of hemoglobin •Skeletal x-rays •Magnetic resonance imaging (MRI) •Doppler studies •X-rays CARE: •Serious sequelae, such as acute chest syndrome, can lead to immediate death. •*Teach patients to avoid high altitudes* •Maintain adequate fluid intake •Treat infections promptly •*Screening for retinopathy should begin at age 10*. •*Administer immunizations such as pneumococcal, Haemophilusinfluenzae, influenza, and hepatitis.* Hospitalized patients in sickle cell crisis: •*O2 for hypoxia and to control sickling* •Vigilance for respiratory failure •*Rest with DVT prophylaxis: anticoagulants* •Administration of fluids and electrolytes •Transfusion therapy: when aplastic crisis occurs > Chelation therapy with repeat exacerbations Pain management: •*Often pain medication tolerant* •Require continuous and breakthrough analgesia with morphine and hydromorphone Multimodal and interdisciplinary approach •Treat infections •Administer folic acid • *hydroxyurea (Hydrea) is only antisickling agent shown to be clinically beneficial* •*Hematopoietic stem cell transplantation (HSCT) is only available cure*

Heart

Heart > Four chambers > Composed of three layers: §Endocardium §Myocardium §Epicardium §Pericardium §Left ventricular wall 2-3 times thicker than right BLOOD FLOW OF HEART §Systole: Contraction of heart muscle §Diastole: Relaxation of heart muscle §Stroke volume: Amount of blood ejected with each heart beat §Cardiac output: Amount of blood pumped by each ventricle in 1 minute §Normal 4-8 L/min •CO = SV X HR. §Cardiac index: CO divided by body surface area §Normal 2.8-4.2 L/min/m2 §Preload: §Volume of blood in ventricles at end of diastole §Contractility §Afterload: §Peripheral resistance against which left ventricle must pump

Valvular Heart Disease

Heart has Two atrioventricular valves: §Mitral §Tricuspid Two semilunar valves: §Aortic §Pulmonic Types of valvular heart disease depend on: §Valve(s) affected Type of dysfunction: §Stenosis = (constriction/narrowing) forward blood is impeded. §Insuffiency = Regurgitation = backflow RISK FACTORS: HTN Rheumatic fever ineffective endocarditis congenital malformations Marfan syndrome = connective tissue disorder atherolscerosis CLINICAL MANIFESTATIONS: murmur CARE: daily weights O2 fluid and sodium restrictions conserve energy Valve replacement MEDS diuretics ACE ARBS BBlockers CCB Vasodilators Digoxin Anticougulants COMPLICATIONS: HF

PAD

Involves progressive narrowing and degeneration of arteries of upper and lower extremities §*Atherosclerosis is leading cause in majority of cases* §Patients with PAD are more likely to have coronary artery disease and/or cerebral artery disease RISK FACTORS: §Tobacco use §Chronic kidney disease §Diabetes mellitus §Hypertension §Hypercholesterolemia females over 65 CLINICAL MANIFESTATIONS: Classic symptom of PAD -*intermittent claudication:* §Ischemic muscle pain that is caused by a constant level of exercise §Resolves within 10 minutes or less with rest Paresthesia: numbing or tingling in toes or feet. §Thin, shiny, and taut skin §Loss of hair on the lower legs §Diminished or absent pedal, popliteal, or femoral pulses §Pallor of foot with leg elevation §Reactive hyperemia of foot with dependent position Pain at rest decreased cap refill of toes COMPLICATIONS: §Atrophy of skin and underlying muscles §Delayed healing §Wound infection §Tissue necrosis §Arterial ulcers Gangrene may result in amputation compartment syndrome DIAGNOSTIC STUDIES: Doppler ultrasound: Segmental blood pressure Ankle-brachial index (ABI): Done using a hand-held Doppler §Angiography and magnetic resonance angiography DRUG THERAPY: ACE: Ramipril (Altace) Statins Antiplatelet agents: §Aspirin §Clopidogrel (Plavix) Drugs prescribed for treatment of intermittent claudication: Cilostazol (Pletal): §Inhibits platelet aggregation §↑ Vasodilation • Contraindicated in patients with heart failure of any severity. Pentoxifylline (Trental): §Improves deformability of RBCs and WBCs §Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity CARE: Exercise Reduce calories and salt

Hemochromatosis

Iron overload disorder: •Primarily caused by a genetic defect •May occur secondary to other diseases Genetic link: •Increased intestinal iron absorption •Increased tissue iron deposition

Anemia

*A deficiency in: •Number of erythrocytes (RBCs) •Quantity of hemoglobin •Volume of packed RBCs (hematocrit) CAUSES: *blood loss:* Acute: Trauma, GI bleed, ruptured aortic aneurysms Chronic: Bleeding duodenal ulcer, colorectal cancer, liver disease. *impaired production of erythrocytes:* Deficient nutrients: iron, cobalamin, folic acid. Decreased erythropoietin decreased iron availability *increased destruction of erythrocytes:* Hemolysis: Sickle cell disease meds -- methyldopa (Aldomet) Incompatible blood Trauma (Cardiopulmonary bypass) Rapid metabolic activitY: pregnancy adolescents infection age RBC FUNCTION: •Transport oxygen (O2) from lungs to systemic tissues •Carry carbon dioxide from tissues to lungs •Because RBCs transport oxygen (O2), erythrocyte disorders can lead to tissue hypoxia. •This hypoxia accounts for many of the signs and symptoms of anemia. •Not a specific disease •Manifestation of a pathologic process Diagnosed based on: •Complete blood count (CBC) •Reticulocyte count •Peripheral blood smear CLASSIFICATION: Morphologic: •Cellular characteristics: erythrocyte size and color Etiologic: •Underlying cause

ITP, TTP, HIT

*Immune Thrombocytopenic Purpura (ITP):* •*Most common acquired thrombocytopenia* •Syndrome of *abnormal destruction of circulating platelets* •Primarily an *autoimmune disease* •Decreased platelet production contributes to ITP. •Sometimes infection, such as Helicobacter pylorior viral infection, contribute to this disorder. *Can result in serious hemorrhages* RISK FACTORS: Females 20-50 Secondary conditions (meds, viruses - HIV, Hep C) Recent viruses (children only) DRUG THERAPY: *corticosteroids, splenectomy (if don't respond to meds), immunosuppressants, or thrombopoietin receptor agonists.* *Thrombotic Thrombocytopenic Purpura (TTP):* •*platelets abnormally clump together in capillaries due to AUTOIMMUNE reaction from platelet aggregation; inappropriate clotting occurs; can lead to kidney failure, MI, stroke; fatal in 3 months if untreated* •Called TTP-HUS as it is most always associated with hemolytic-uremic syndrome: •*characterized by hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever (in the absence of infection), and renal abnormalities; not all features are always present in all patients.* •Associated with enhanced aggregation of platelets that form into microthrombi: •The microthrombi deposit in arterioles and capillaries. RISK FACTORS: other immune disorders CAUSES: •Caused by plasma enzyme deficiency •Primarily in previously healthy adults •Idiopathic or from drug toxicities Medical emergency: •*Bleeding and clotting occur simultaneously* DRUG THERAPY: •Therapy initiated if platelets ↓30,000/μL: Anti platelet meds: *Aspirin, alprostadil, plicamycin* *Immunosuppressive therapy decreases the intensity of complications* *Heparin-Induced Thrombocytopenia (HIT):* •*Associated with increased use of heparin; low platelet count* •Life-threatening •Two major responses to an immune-mediated response to heparin: •*Platelet destruction* •Vascular endothelial injury •*Develops 5-10 days after heparin therapy is started* •*Platelet count drops 50% from baseline* •Venous thrombosis is major clinical problem •Arterial thrombosis can also develop •*DVT and PE often result* RISK FACTORS: Female *Receving heparin over 1 week* Post surgical thromboprophylaxis CARE: •*Permanently stop all heparin including heparin flushes* •Note clearly on medical record •Start patient on a direct thrombin inhibitor •*Start warfarin (Coumadin) when platelet count reaches 150,000/μL* For severe clotting: •Plasmapheresis to clear platelet-aggregating IgG from the blood •Protamine sulfate to interrupt circulating heparin •Thrombolytic agents to treat thromboembolic events •Surgery to remove clots DRUG THERAPY: *Anticoagulants with direct thrombin inhibitor (argatroban, leiprudin, bivalirduin)* *Disseminated intravascular coagulation DIC)* *Complex disorder caused by overstimulation of clotting and anti-clotting mechanisms occur at the same time*; leads to overwhelming and diffuse hemorrhage; *oozing from puncture sites or development of petechiae may be initial clues of coagulopathy.* RISK FACTORS: DIC secondary to other complications: *Septicemia* Cardiopulmonary arrest Trauma Obstetic complications Cancer Allergic reactions CARE: A complication of septic shock. Thousands of small clots form leading to hypoxemia. *Platelets and other clotting factors such as fibrinogen are depleted and pt is at increased risk for hemorrhage*. Develops petechiae, ecchymoses, and blood can leak from membranes and puncture sites. Assess patients on blood transfusion Adminster platelets, clotting factors, and other blood products Monitor PT, PTT, blood fibrinogen, fibrin Assess for further indications of bleeding from mucous membranes, ventipuncture sites, gums, and around IV caths. Apply pressure to leaking IV sites. Correct underlying cause (sepsis, malignancy, hemorrhage). Prevent organ damage Monitor for manifestations of micro emboli (Cyantoic nail beds, pain) DRUG THERAPY: *Anticoagulants (heparin): used to decreased micro clots from forming and using up clotting factors.* CLINICAL MANIFESTATIONS: ALL Unusual spontaneous bleeding from gums and nose Oozing, trickling of blood from incisions or lacerations Petichae and eccymoses Hematuria Excessive bleeding from puncture sites Tachycardia Hypotension Diaphoresis Organ failure Respiratory distress HIT = Redness, warmth and swelling over lower extremities DIAGNOSTIC STUDIES: Hemoglobin : ↓ with DIC & ITP Platlet level: ↓ with DIC, ITP & TTP Fibrinogen : ↓ with DIC PT: increased with DIC D Dimer: increased with DIC Blood typing and cross match CARE: Transfuse blood Avoid NSAIDS O2 NO needles avoid Valsalva maneuver (could cause cerebral hemorrhage)

Hematology

= Study of blood and blood-forming tissues •Bone marrow •Blood •Spleen •Lymph system •Blood cells make up 45% of blood *Erythrocytes (RBCs):* •Oxygen transportation •Transport O2 and CO2 •Hemoglobin = iron + protein •Oxyhemoglobin= O2 + iron *Leukocytes (WBCs):* •Protection from infection *Thrombocytes (platelets):* •Promote coagulation Spleen: •Located in the upper left quadrant next to kidney •Functions can be classified as •1. Hematopoietic: Able to produce RBCs during fetal development •2. Filtration •Removes old and damaged RBCs from circulation •Removes hemoglobin from RBCs and returns iron component to bone marrow for reuse •Filters out bacteria, especially encapsulated organisms •3. Immunologic: Contains a rich supply of lymphocytes, monocytes, and stored immune globulins •4. Storage: Stores RBCs and approximately 30% of total mass of platelets Lymph System: •*Returns excess interstitial fluid to blood to prevent or reduce edema* Lymph nodes: •Primary function is filtration of pathogens and foreign particles carried by lymph fluid •Located both superficially and deep Liver: •Functions as a filter •Produces all procoagulants essential to hemostasis and blood coagulation •Stores excess iron •Produces hepcidin, which regulates iron balance

Leukemia

A group of malignant disorders affecting the blood and blood-forming tissues of: •Bone marrow •Lymph system •Spleen •Occurs in all age groups •Accumulation of dysfunctional cells due to loss of regulation in cell division CAUSES: •No single cause •Combination of genetic and environmental influences •Oncogenes, or abnormal genes, cause many types of cancers CLASSIFICATION: Acute versus Chronic •Cell maturity and nature of disease onset •*Acute: Clonal proliferation of immature hematopoietic cells* •*Chronic: Mature forms of WBC and onset is more gradual* •*Based on type of WBC!!!* CLINICAL MANIFESTATIONS: •Varied but usually related to: •*Bone marrow failure* •Overcrowding by abnormal cells •Inadequate production of normal marrow elements •Formation of leukemic infiltrates Inadequate marrow elements cause: •Anemia •Thrombocytopenia •Low to high number and altered function of WBCs •Splenomegaly •Hepatomegaly •Leukemic cells may cause: •Lymphadenopathy •Bone pain •Meningeal irritation •Oral lesions •Solid masses (chloromas) *Leukostasis:* •Life-threatening complication •*Caused by a high leukemic WBC count in peripheral blood* •Blood thickens and blocks circulatory pathways •Leukemic white cell count in the peripheral blood is >100,000/µL. DIAGNOSTIC STUDIES: •Peripheral blood evaluation •*Bone marrow examination* To determine the presence of leukemic cells outside of blood and bone marrow: •Lumbar puncture •CT scan Diagnostic Findings: •WBC may be normal or abnormal •Anemia •↓ Hct and Hgb •Thrombocytopenia •*Philadelphia chromosome* •Hypercellularbone marrow aspirate or biopsy CARE: •Initial goal is to attain remission

Answer: A Rationale: Troponin is the biomarker of choice in the diagnosis of myocardial infarction. Troponin is a myocardial muscle protein released into the circulation after injury. Troponin levels peak at 10 to 24 hours.

A patient arrives at an urgent care center after experiencing unrelenting substernal and epigastric pain and pressure for about 12 hours. The nurse reviews laboratory results with the understanding that at this point in time, a myocardial infarction would by indicated by peak levels of a.Troponin T. b.Homocysteine. c.Creatine kinase-MB. d.Type b natriureticpeptide.

Answer: B Rationale: Immediate treatment for ventricular fibrillation is the initiation of cardiopulmonary resuscitation, followed by the use of defibrillation and definitive drug therapy according to advanced cardiac life support guidelines.

A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to a.Perform defibrillation. b.Initiate cardiopulmonary resuscitation. c.Prepare for synchronized cardioversion. d.Administer IV antidysrhythmic drugs per protocol.

Answer: C Rationale: Traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation is a relative contraindication for the administration of fibrinolytic therapy.

A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation. When reviewing the health care provider's admission orders, which order should the nurse question? a.Oxygen at 4 L/min per nasal cannula b.Morphine sulfate 2 mg IV every 10 minutes until the pain is relieved c.Tissue plasminogen activator (tPA) 100 mg IV infused over 3 hours d.IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3 to 5 minutes

Answer: C Rationale: Afterload is affected by size of the ventricle, wall tension, and arterial blood pressure.

A patient is receiving a drug that decreases afterload. To evaluate the patient's response to this drug, what is mostimportant for the nurse to assess? a.Heart rate b.Lung sounds c.Blood pressure d.Jugular venous distention

Answer: D Rationale: ST elevation on ECG indicates myocardial ischemia or injury with partial or total occlusion of a coronary artery. This assessment finding requires immediate action. Actions would include assessment for chest pain, 12-lead ECG, administration of nitroglycerin or morphine, and notification of the health care provider. Option 1 would need further assessment but is not critical unless the patient is symptomatic (chest pain, shortness of breath, hypotension, etc.). Options 2 and 3 are normal findings.

A patient returns to the cardiac observation area following a cardiac catheterization with coronary angiography. Which assessment would require immediate action by the nurse? a.Pedal pulses are 2+ bilaterally. b.Apical pulse is 54 beats/minute. c.Mean arterial pressure is 72 mm Hg. d.ST-segment elevation develops on the ECG

Answer: B Rationale: The patient is experiencing acute decompensated heart failure with symptoms of both right- and left-sided heart failure. Left-sided heart failure prevents normal, forward blood flow and causes pulmonary congestion. Right-sided heart failure causes a backup of blood and results in venous congestion.

A patient with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. Assessment findings include pitting edema in both ankles, BP 170/100 mm Hg, pulse 92 beats/minute, and respirations 28 breaths/minute. Which explanation, if made by the nurse, is most accurate? a."The assessment indicates that venous return to the heart is impaired, causing a decrease in cardiac output." b."The manifestations indicate impaired emptying of both the right and left ventricles, with decreased forward blood flow." c."The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand." d."The patient's right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation."

Answer: B Rationale: Left-sided heart failure will prevent normal blood flow and will cause blood to back up into the left atrium and into the pulmonary veins. The increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then the alveoli, which manifests as pulmonary congestion and edema. The most important assessment to determine if the drugs are improving the patient's condition is to auscultate lung sounds. The other assessments are important, but the best indicator of improvement of left ventricular function is a reduction in adventitious lung sounds (crackles).

A patient with left-sided heart failure is prescribed oxygen at 4 L/min per nasal cannula, furosemide (Lasix), spironolactone (Aldactone), and enalapril (Vasotec). Which assessment should the nurse complete to best evaluate the patient's response to these drugs? a.Observe skin turgor b.Auscultate lung sounds c.Measure blood pressure d.Review intake and output

Answer: A Rationale: Peripheral neuropathy is caused by diminished perfusion to neurons and results in loss of both pressure and deep pain sensations. The patient may not notice lower extremity injuries. Neuropathy increases susceptibility to traumatic injury and results in delay in seeking treatment.

A patient with peripheral artery disease has marked peripheral neuropathy. An appropriate nursing diagnosis for the patient is a.Risk for injury related to decreased sensation. b.Impaired skin integrity related to decreased peripheral circulation. c.Ineffective peripheral tissue perfusion related to decreased arterial blood flow. d.Activity intolerance related to imbalance between oxygen supply and demand.

Answer: C Rationale: Side effects of antihypertensive drugs are common and may be so severe or undesirable that the patient does not comply with therapy.

A patient's BP has not responded consistently to prescribed drugs for hypertension. The first cause of this lack of responsiveness the nurse should explore is a.progressive target organ damage. b.the possibility of drug interactions. c.the patient not adhering to therapy. d.the patient's possible use of recreational drugs.

Answer: D Rationale: Signs of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath.

A patient's cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit a.Palpitations. b.Hypertension. c.Warm, flushed skin. d.Shortness of breath.

Acute Decompensated Heart Failure (ADHF)

ADHF CLINICAL MANIFESTATIONS: §Sudden onset of signs and symptoms of HF §Requires urgent medical care §Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures Early→ increased pulmonary venous pressure §Increase in the respiratory rate §Decrease in Pao2 Later→ interstitial edema §*Tachypnea* §*Further progression → alveolar edema* §Respiratory acidemia §Based on hemodynamic and clinical status, patients can be categorized into one of four groups 1.Dry-warm 2.Dry-cold 3.*Wet-warm (most common)* 4.Wet-cold •A patient is "wet" due to volume overload (e.g., congestion, dyspnea), but "warm" due to adequate perfusion (warm skin, positive pulses). §*Can manifest as pulmonary edema* NEXT SLIDE §Life-threatening situation - alveoli fill with fluid §Most commonly associated with left-sided HF DRUG THERAPY: *Diuretics:* §Decrease volume overload (preload) §Loop diuretics - Furosemide (Lasix) *Vasodilators:* §Reduce circulating blood volume and improve coronary artery circulation §IV nitroglycerin §Sodium nitroprusside §Nesiritide (Natrecor) *Morphine:* §Reduces preload and afterload §Relieves dyspnea and anxiety *Positive inotropes:* §β-agonists (dopamine, dobutamine, norepinephrine [Levophed]) §Phosphodiesterase inhibitor (milrinone) §Digitalis -- contraindicated in hypokalemia. Digoxin -- take apical pulse for 1 full minute. hold if HR under 60. Monitor for N/V.

HTN

CLINICAL MANIFESTATIONS: §"Silent killer" Symptoms of severe hypertension: §Fatigue §Dizziness §Palpitations §Angina §Dyspnea COMPLICATIONS: Target organ diseases occur most frequently in: §Heart (hypertensive heart disease) §Brain: (cerebrovascular disease) §Peripheral vascular disease §Kidneys (nephrosclerosis) §Eyes (retinal damange) DIAGNOSTIC STUDIES: §Measurement of BP §Urinalysis §BUN and serum creatinine §Creatinine clearance §Serum electrolytes, glucose §Serum lipid profile §Uric acid levels: •*Uric acid levels establish a baseline, because the levels often rise with diuretic therapy.* §ECG §Echocardiogram Ambulatory blood pressure monitoring (ABPM): §Noninvasive, fully automated system that measures BP at preset intervals over 24-hour period §Teach patient to hold arm still and keep diary §Many applications for use TEACHING: Weight reduction: §*Weight loss of 22 lb (10 kg ) may decrease SBP by approx. 5 to 20 mm Hg* §Calorie restriction and physical activity *DASH eating plan:* §*Fruits, vegetables, fat-free or low-fat milk, whole grains, fish, poultry, beans, seeds, and nuts* Dietary sodium reduction: §< 2300 mg/day for healthy adults §<1500 mg/day for: §African Americans §Middle-aged and older §Those with hypertension, diabetes, or chronic kidney disease Moderation of alcohol intake Physical activity: §Moderate-intensity aerobic activity, at least 30 minutes, most days of the week Smoking cessation Decrease Stress DRUG THERAPY: *Diuretics: first line of therapy = hydrochlorothiazide* Adrenergic-inhibiting agents = clonidine (Catapress) Direct vasodilators Calcium Channel Blockers = diltiazam, verapamil, nifedipine ACE inhibitors = prils ARBS = sartans Beta-blockers. = olol Identify, report, and minimize side effects: §Orthostatic hypotension §*Sexual dysfunction: main reason ppl don't adhere to medications.* §Dry mouth §Frequent urination §*Time of day to take drug: diuretics in morning to decrease frequent awakening.* GERIATRICS: §*BP goal for people > 60 is < 150/90* Preferred antihypertensive drugs: §Thiazide diuretic §Calcium channel blockers §ACE inhibitors or ARBs §Caution use of NSAIDS

Types of Leukemia

Acute Myelogenous Leukemia (AML): •25% of all leukemias •*80% of the acute leukemias in adults* •Abrupt, dramatic onset •Serious infection or abnormal bleeding •Uncontrolled proliferation of myeloblasts •*Hyperplasia of bone marrow and spleen* Acute Lymphocytic Leukemia (ALL): •*Most common type of leukemia in children* •20% of acute leukemia in adults •Immature, small lymphocytes proliferate in the bone marrow •B cell origin Signs and symptoms may appear: •Abruptly: > Fever > Bleeding •Insidiously: > Progressive weakness, fatigue, pain, bleeding tendencies •CNS manifestations are common = serious problem Chronic Myelogenous Leukemia (CML): •Excessive mature neoplastic granulocytes in bone marrow •Move into peripheral blood in massive numbers •Ultimately infiltrate liver and spleen •*Philadelphia chromosome:* > Genetic marker > Present in >90% to 95% CML patients •Chronic, stable phase •Followed by acute, aggressive (blastic) phase Chronic Lymphocytic Leukemia (CLL): •*Most common leukemia in adults* •*Production and accumulation of functionally inactive but long-lived, mature-appearing lymphocytes* •B cell involvement •Lymphadenopathy is present throughout body •Complications from early-stage CLL are rare •May develop as disease advances •Pain, paralysis from pressure caused by enlarged lymph nodes

Answer: A Rationale: Thrombocytopenia is a platelet count of less than 100,000/μL.

B.C is diagnosed with thrombocytopenia. To evaluate the effectiveness of her treatment, the nurse plans to monitor the: a.platelet count. b.prothrombintime. c.partial thromboplastintime. d.international normalized ratio (INR).

Blood Pressure

BP = CO x SVR •blood pressure is a measure of the pressure exerted by blood against the walls of the arterial system. Pulse pressure: §Difference between SBP and DBP §Normally about 1/3 of the SBP Mean arterial pressure: §Average pressure within arterial system that is felt by organs in body §MAP = (SBP + 2 DBP) ÷ 3

Hypertensive Crisis

BP over 180/110 Hypertensive urgency: §Develops over hours to days §May not require hospitalization *ORAL clondine (Catapress) or amlodipine (Norvasc)* Hypertensive emergency: §Very severe problems can result if prompt treatment is not obtained: These include encephalopathy, intracranial or subarachnoid hemorrhage, heart failure, MI, renal failure, dissecting aortic aneurysm, and retinopathy. §Rate of rise more important than absolute value *Usually due to under-medicated or non-adherence to meds* •*The difference between a hypertensive urgency and emergency is the absence or presence of target organ damage.* CLINICAL MANIFESTATIONS: Hypertensive encephalopathy: §*Headache, nausea/vomiting, seizures, confusion, coma* *Retinal Damage* Renal failure Cardiac decompensation: §MI, HF, pulmonary edema Aortic dissection The neurologic changes are often similar to those related to a stroke. However, a hypertensive crisis does not show focal or lateralizing signs often seen with a stroke *SODIUM NITROPRUSSIDE IV* CARE: §Hospitalization §*IV drug therapy: titrated to MAP; The initial goal is to decrease MAP by no more than 20% to 25%, or to decrease MAP to 110 to 115 mm Hg; Assess the patient's BP and HR every 2 to 3 minutes during the initial administration of these drugs.* §Monitor cardiac and renal function; Monitor the ECG for dysrhythmias and signs of ischemia or MI. Measure urine output hourly to assess renal perfusion. §Neurologic checks §Determine cause §Education to avoid future crisis Quiet room 20-30 minutes lowers BP

Blood Types

Blood type O is universal donor. Blood type AB is universal receiver; can get from A, B, O, AB. Blood type A can get from A or O Blood type B can get B or O O blood type can only get O •Blood typing and Rh factor •Blood group antigens •Rh system based on a third antigen, D •Rh+ have antigen D •Rh- do not •*Coombs test determines Rh status* •Significant with transfusions and during childbirth

Coronary Artery Disease CAD

CAD: Chronic stable angina & Acute coronary syndrome Patients with CAD can be asymptomatic or develop chronic stable angina (or chest pain). CAD may also evolve to more serious conditions of unstable angina (UA) and myocardial infarction (MI), which are called acute coronary syndrome (ACS)." •Coronary artery disease is a type of blood vessel disorder that is included in the general category of atherosclerosis. •*Atherosclerosis* Begins as soft deposits of fat that harden with age Referred to as "*hardening of arteries"* Atheromas (fatty deposits) prefer coronary arteries •Atherosclerosis is major cause of CAD; •Endothelial injury and inflammation play a central role in the development of atherosclerosis. •*C-reactive protein (CRP)* Nonspecific marker of inflammation Increased in many patients with CAD Chronic exposure to CRP linked with unstable plaques and oxidation of LDL cholesterol RISK FACTORS: •Nonmodifiable risk factors: Age Gender: middle aged men Ethnicity: African Americans Family history Genetic predisposition •Major modifiable risk factors Elevated serum lipids: total and LDL; cholesterol over 200; triglycerides over 150. HTN Tobacco Use Physical inactivity Obesity Diabetes Metabolic Syndrome: insuline resistance Homocysteine level: Increased levels increase risk of CVD. CARE: physical fitness •Nutritional therapy ↓ Saturated fats and cholesterol ↓ Red meat, egg yolks, whole milk ↑ Complex carbohydrates and fiber ↑Omega-3 fatty acids *"low-saturated-fat, high-fiber diet"* DRUG THERAPY: •Lipid-lowering drug therapy: If diet and exercise ineffective *Statins: Simvastatin (Zocor)* •Inhibit cholesterol synthesis, decrease LDL, increase HDL •Monitor for liver damage and myopathy "Increased risk for rhabdomyolysis when also used with gemfibrozil (Lopid) or niacin (Niaspan)•Signs of rhabdomyolysis: ↑ creatine kinase levels, muscle pain" Take at bedtime. *Niacin*: •Lowers LDL and triglyceride by inhibiting synthesis •Increases HDL •Flushing, pruritus, GI side effects, orthostatic hypotension "Patient can premedicate with aspirin 30 minutes before taking to reduce flushing" *Fibric acid derivatives Gemfribozil (Lopid):* •Decrease triglycerides and increase HDL •GI side effects "May increase the risk of bleeding in patients taking warfarin (Coumadin) •May increase the effects of antihyperglycemic drugs (e.g., repaglinide" •Increase lipoprotein removal: *Bile acid sequestrants:* •Increase conversion of cholesterol to bile acids •GI side effects; bind with other drugs •Decrease cholesterol absorption Lowers total and LDL *Ezetimibe (Zetia):* •Decrease absorption of dietary and biliary cholesterol •*Antiplatelet therapy:* Aspirin low dose 81 mg for at least 10 years. Clopidogrel (Plavix) CLINICAL MANIFESTATIONS: •Chronic and progressive disease •O2 demand > O2 supply → myocardial ischemia: lead to chest pain (angina) •Angina = clinical manifestation:

Diagnostic Studies: Cardiovascular System.

CARDIAC BIOMARKERS: > Troponin §Troponin T (cTnT) §Troponin I (cTnI) §Rises within 4-6 hours, peaks 10-24 hours, detected for up to 10-14 days •Troponin is the biomarker of choice in the diagnosis of acute coronary syndrome (ACS). Normally the level in the blood is very low, so a *rise in level is diagnostic of myocardial infarction (MI) or injury* > Creatinekinase (CK) §Three isoenzymes §CK-MB cardiac specific: CK-MB rise is specific for MI or injury. §Rises in 3-6 hours, peaks in 12-24 hours, returns to baseline within 12-48 hours > C-Reactive protein (CRP) is a *protein produced by the liver during periods of acute inflammation*. §Marker for inflammation §Linked to *atherosclerosis* > Homocysteine •is an amino acid that is produced during protein catabolism. Elevated Hcy levels can be either *hereditary or acquired from dietary deficiencies of vitamin B6, vitamin B12, or folate* §Elevated levels increased risk for CVAD, peripheral vascular disease (PVD), and stroke > Cardiac natriuretic peptide markers Three types: §Atrial natriuretic peptide (ANP): atrium §B-type natriuretic peptide (BNP): ventricles §C-type natriuretic peptide: endothelial and rental epithelial cells. §*Increased levels of BNP levels signify heart failure; BNP is the marker of choice for distinguishing a cardiac or respiratory cause of dyspnea* §NT-pro-BNP: is also secreted in the ventricles and is more sensitive but less specific than BNP as a diagnostic marker of heart failure

Pulmonary Edema

CLINICAL MANIFESTATIONS: §Anxious, pale, cyanotic §Cool and clammy skin §Dyspnea §Orthopnea §Tachypnea §Use of accessory muscles §*Cough with frothy, blood-tinged sputum* §Crackles and wheezes §Tachycardia §Hypotension or hypertension §Abnormal S3 or S4 reduced urine output CARE: High fowlers O2 Morphine IV IV loop dietetics = furosemide vitals q 15 mins I&O's restrict fluid intake report swelling of feet or ankles or SOB, or angina DRUG THERAPY: Diueritcs Morphine Vasodilators = Nitroglycerin, sodium nitroprusside Digoxin Antihypertensives = ACE, BBlockers

ANEMIA

CLINICAL MANIFESTATIONS: •Caused by body's response to tissue hypoxia •Hemoglobin (Hgb) levels are used to determine severity of anemia MILD AMENIA: HGB = 10-12 (100-120) •palpitations, dyspnea, and mild fatigue. MODERATE AMENIA: HGB = 6-10 (60-100) the above cardiopulmonary symptoms are increased. The patient may experience them while resting, as well as with activity. SEVERE AMENIA HGB = LESS THAN 6 (60) involves multiple body systems SKIN: Pallor: •↓ Hemoglobin •↓ Blood flow to the skin Jaundice: •↑ Concentration of serum bilirubin the sclerae of the eyes and mucous membranes should be evaluated for jaundice Pruritus: •↑ Serum and skin bile salt concentrations CARDIOPULMONARY: MI HF RSHF CARE: rest for fatigue •Encourage increased intake of foods high in iron.

Diagnostic Studies: Cardio

CXR EKG §Nuclear cardiology §*MUGA scan*: cardiac blood pool scan; This test provides information on wall motion during systole and diastole, heart valves, and EF §Stress perfusion imaging: used with exercise to see blood flow changes with activity. §IV medications to dilate coronary arteries and simulate exercise effects: regadenoson (Lexiscan), dipyridamole, or adenosine (Adenocard) §SPECT = Used to determine size or risk of infarction and to determine infarction size. §PET stress testing §Cardiovascular magnetic resonance imaging (CMRI) §Cardiac computed tomography §CT angiography (CTA) §Calcium-scoring screening\ Cardiac catheterization: §Right-sided to measure pressures of the pulmonary artery: to assess function of left side of the heart. §Left-sided to evaluate coronary arteries Coronary angiography: is done with a left-sided heart catheterization. §Uses contrast medium to identify coronary blockages "Procedure is done by insertion of catheter into a vein (for right side of heart) and/or an artery (for left side of heart)" Intravascular ultrasound: §Done with coronary angiography Fractional flow reserve: §Special wire measures pressure and flow in coronary artery Electrophysiology study: §Provides information on cardiac conduction

Anemia of Chronic Disease: Anemia of Inflammation

Caused by: •Chronic inflammation •Autoimmune and infectious disorders = HIV, hepatitis, malaria •Heart failure •Malignant diseases •Bleeding episodes Associated with: •Underproduction of RBCs •Mild shortening of RBC survival > Normocytic, normochromic, and hypoproliferativeRBCs •Usually a mild anemia but can become severe if the underlying disorder is untreated •This type of anemia, which usually develops after 1 to 2 months of disease activity, has an immune basis. Anemia of chronic disease findings: •↑ Serum ferritin •↑ Iron stores •Normal folate and cobalamin levels Treating underlying cause is best treatment then: •Rarely blood transfusions; maybe if severe. •Conservative use of erythropoietin therapy

Hemolytic Anemia

Destruction or hemolysis of RBCs at a rate that exceeds production •Caused by problems intrinsic or extrinsic to the RBCs •Intrinsic forms are usually *hereditary* and result from defects in RBCs themselves •RBCs are normal in acquired forms that are more common. Damage is caused by external factors. •Extrinsic: The spleen is the primary site of destruction of RBCs that are old, defective, or moderately damaged. CLINICAL MANIFESTATIONS: Specific manifestations including: •*Jaundice due to increase in billrubin levels.* •Enlargement of the spleen and liver •Maintenance of renal function is a major focus of treatment

Left sided heart failure

Most common form of HF Results from inability of LV to: §Empty adequately during systole §Fill adequately during diastole Increased pulmonary pressure causes fluid leakage →→ *pulmonary congestion* and edema RISK FACTORS: HTN CAD, angina, MI Valvular disease CLINICAL MANIFESTATIONS: Dyspnea, orthopnea, nocturnal dyspnea fatigue S3 (gallop) *PULMONARY CONGESTION: dyspnea, crackles, cough* *Frothy sputum: blood-tinged* AMS *Oliguria*

Hypertension Classification

Normal = 120/80 Prehypertension = 120/80 to 139/89 Hypertension Stage 1 = 140/90 - 159/99 Hypertension Stage 2 = > 160/100 Primary hypertension: §Also called essential or idiopathic hypertension §Elevated BP *without an identified cause* §90% to 95% of all cases §Exact cause unknown but several contributing factors = *weight, diabetes, tobacco use, alcohol intake, increase sodium intake.* §Persistently increased SVR Risk factors: Primary HTN §Age: after 50 §Alcohol §Tobacco use §Diabetes mellitus §Elevated serum lipids: total and LDL §Excess dietary sodium §Gender: young men, and women over 64. §Family history §Obesity §Ethnicity: African Americans §Sedentary lifestyle §Socioeconomic status §Stress Secondary hypertension: §*Elevated BP with a specific cause* §5% to 10% of adult cases §Clinical findings relate to underlying cause §Treatment aimed at removing or treating cause

Right Sided Heart Failure

RV fails to pump effectively §Fluid backs up in venous system §Fluid moves into tissues and organs (peripheral edema, ascites, hepatomegaly, JVD) §*Left-sided HF is most common cause* §Other causes include RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy) CLINICAL MANIFESTATIONS: *JVD* *edema (legs, ankles, sacrum)* Abdominal distention, *ascites* fatigue/weakness nausea/anorexia *polyuria* liver enlargement (hepatomegaly) & tenderness weight gain

Thrombocytopenia

Reduction of platelets *below 150,000*/μl(150 × 109/L). •Results in abnormal hemostasis > *Prolonged or spontaneous bleeding* •*Primarily an acquired disorder* •*Commonly from ingestion of high doses of certain drugs: aspirin* CAUSES: NEXT SLIDE •Inherited *Acquired:* •Immune thrombocytopenia purpura (ITP) •Thrombotic thrombocytopenia purpura (TTP) •Heparin-induced thrombocytopenia (HIT) CLINICIAL MANIFESTATIONS: •Patients are often asymptomatic •Most common symptom is *mucosal or cutaneous bleeding:* •Petechiae- microhemorrhages •Purpura- bruise from numerous petechiae •Ecchymoses- larger lesions from hemorrhage •Clinical Manifestations •Prolonged bleeding after routine procedures: •Internal bleeding may manifest as weakness, fainting, dizziness, tachycardia, abdominal pain, or hypotension •*Hemorrhage is a major complication:* •Insidious or acute •Internal or external DIAGNOSTIC STUDIES: •↓ Platelet count: •*Prolonged bleeding <50,000/μL* •*Spontaneous Hemorrhage ↓20,000/μL* •Peripheral blood smear •Medical history •Clinical examination •Lab parameter comparisons •*Platelet transfusions are generally not recommended until the count is below 10,000/μL(10 × 109/L) unless the patient is actively bleeding.* •Bone marrow exam can identify production problems as the cause Can be normal: PT/INR For warfarin patients. INR = 2-3. PT = 11-13.5 seconds. Antidote = Vitamin K PTT = For heparin. 45-55 seconds. Antidote = Protamine Sulfate. CARE: •*Avoid aspirin* and other medications that affect platelet function or production For decreased platelet production: •Treat with *corticosteroids* if precipitating factor is unknown •Platelet transfusions for life-threatening hemorrhage •*Avoid IM injections* •If subcutaneous injection is unavoidable, use small-gauge needles and application of pressure or ice packs after •Closely monitor platelet count, coagulation studies, Hgb, and Hct

Acquired Hemolytic Anemia

Results from hemolysis of RBCs from extrinsic factors: •Physical destruction •Antibody reactions •Infectious agents and toxins Physical destruction of RBCs results from exertion of extreme force on cells: •Hemodialysis •Extracorporeal circulation used in cardiopulmonary bypass •Prosthetic heart valves •Abnormal vessels RBCs can be fragmented and destroyed as they try to pass through abnormal arterial or venous microcirculation •Excessive platelet aggregation and/or fibrin polymer formation > Seen in thrombotic thrombocytopenic purpura (TTP) and disseminated intravascular coagulopathy (DIC) •Antibodies may destroy RBCs by mechanisms involved in antigen-antibody reactions CAUSES: INFECTIOUS AGENTS: Cause hemolysis in 3 ways: •Invade the RBC and destroy its contents > Parasites such as in malaria •Release hemolytic substances >Clostridium perfringens •Generate an antigen-antibody reaction > Mycoplasma pneumoniae •Various agents may be toxic to RBCs and cause hemolysis. These hemolytic toxins involve chemicals such as oxidative drugs, arsenic, lead, copper, and bee stings or spider bites. CARE: •Supportive care until the causative agent can be eliminated or made less injurious •Emergency preparedness is essential for potential hemolytic crises > Hydration, electrolyte replacement, corticosteroids, blood products, splenectomy •Folic acid replacement and immunosuppressive agents for chronic conditions

Diagnostic Studies: Cardiovascular System

Serum Lipids: §Triglycerides §Cholesterol §Phospholipids Lipoprotein: §Lipids must bind to protein to circulate in blood Four classes of lipoprotein §Chylomicrons §Low-density lipoproteins (LDLs): bad cholesterol §High-density lipoproteins (HDLs): good cholesterol §Very-low-density lipoproteins (VLDLs) § Elevated Triglycerides and LDL risk factor: CVD § HDL decreases risk §Cholesterol: HDL ratio = A risk assessment is calculated by comparing the total cholesterol to HDL ratio over time. An increase in the ratio indicates increased risk.

Leukemia: Chemo & other treatments

Stages of chemotherapy: •Induction = •is *aggressive* treatment that seeks to eventually restore normal hematopoiesis on bone marrow recovery. •Patient may become critically ill •Postinduction or postremission (consolidation) = Intensification therapy •High-dose therapy •May be given after induction therapy •Drugs that target cell in a different way than those administered during induction may be added. Consolidation therapy: •Started after remission is achieved •Eliminate remaining leukemic cells that may not be pathologically evident Maintenance = > Lower doses of the same drugs given every 3 to 4 weeks •Goal is to keep body free of leukemic cells Combination chemotherapy: •Mainstay treatment •Three purposes •↓ Drug resistance •↓ Drug toxicity using multiple drugs •Interrupt cell growth at multiple points •Corticosteroids •Radiation therapy > Total body radiation in preparation for bone marrow transplantation > Organ- or field-specific such as liver or spleen •Immunotherapy and targeted therapy Stem Cell Transplantation

Answer: B Rationale: Administration of furosemide increases excretion of potassium and may cause hypokalemia. The risk for digitalis toxicity increases if potassium levels are below normal and digoxin is administered. Signs and symptoms of digitalis toxicity include anorexia, nausea and vomiting, visual disturbances (such as "yellow" vision), and dysrhythmias.

The home care nurse visits a patient with chronic heart failure who is taking digoxin (Lanoxin) and furosemide (Lasix). The patient complains of nausea and vomiting. Which action is most appropriate for the nurse to take? a.Perform a dipstick urine test for protein. b.Notify the health care provider immediately. c.Have the patient eat foods high in potassium. d.Ask the patient to record a weight every morning.

Answer: B Rationale: Rapid cardiopulmonary resuscitation and prompt defibrillation (with an automated external defibrillator) and early advanced cardiac life support can produce high long-term survival rates for a witnessed arrest.

The most significant factor in long-term survival of a patient with sudden cardiac death is a.Absence of underlying heart disease. b.Rapid institution of emergency services and procedures. c.Performance of perfect technique in resuscitation procedures. d.Maintenance of 50% of normal cardiac output during resuscitation efforts.

Answer: C Rationale: Monounsaturated fats are found in natural foods such as nuts and avocados, and are the main component of tea seed oil and olive oil (oleic acid). Canola oil is 57% to 60% monounsaturated fat, olive oil is about 75% monounsaturated fat, and tea seed oil is commonly more than 80% monounsaturated fat. Other sources include macadamia nut oil, grapeseed oil, groundnut oil (peanut oil), sesame oil, corn oil, popcorn, whole grain wheat, cereal, oatmeal, safflower oil, sunflower oil, tea-oil Camellia, and avocado oil. Fat intake should be between 25% and 35% of calories (with most from monounsaturated fats and less from saturated fats); red meats should be reduced or eliminated from the diet. Only fatty fish (such as tuna and salmon) should be included in the diet because fatty fish is high in omega-3 fatty acids.

The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective when the patient says, a."I should not eat any red meat such as beef, pork, or lamb." b."I should have some type of fish at least 3 times a week." c."Most of my fat intake should be from olive oil or the oils in nuts." d."If I reduce the fat in my diet to about 5% of my calories, I will be much healthier."

Answer:c, d, e Rationale: Stage 2 hypertension is diagnosed when systolic blood pressure is greater than or equal to 160 mm Hg or diastolic blood pressure is greater than or equal to 100 mm Hg.

The nurse determines that the patient has stage 2 hypertension when the patient's average blood pressure is (select all that apply) a.150/96 mm Hg. b.155/88 mm Hg. c.172/92 mm Hg. d.160/110 mm Hg. e.182/106 mm Hg.

Answer: C, D Rationale: Stage 1 hypertension is diagnosed when the systolic blood pressure is 140-159 mm Hg or the diastolic blood pressure is 90-99 mm Hg. 182/100 meetsthe criteria for Stage 2.

The nurse determines that which blood pressure would meet the criteria for a diagnosis of stage 1 hypertension (select all that apply)? a.134/84 mm Hg b.138/88 mm Hg c.144/92 mm Hg d.156/96 mm Hg e.182/100 mm Hg

Answer: C Rationale: Rapid cardiopulmonary resuscitation, prompt defibrillation (with an automated external defibrillator), and early advanced cardiac life support can produce high long-term survival rates for a witnessed arrest.

The nurse is caring for a patient who survived a sudden cardiac death. What should the nurse include in the discharge instructions? a."Because you responded well to CPR, you will not need an implanted defibrillator." b."The most common way to prevent another arrest is to take your prescribed drugs." c."Your family members should learn how to perform CPR and practice these skills regularly." d."Since there was no evidence of a heart attack, you do not need to worry about another episode."

Answer: A Rationale: The four major modifiable risk factors for coronary artery disease are elevated serum lipids, hypertension, tobacco use, and physical inactivity. Other risk factors include diabetes mellitus, metabolic syndrome, psychologic states, high levels of homocysteine, and substance abuse.

Which patient is most at risk for developing coronary artery disease? a.A hypertensive patient who smokes cigarettes b.An overweight patient who uses smokeless tobacco c.A patient who has diabetes and uses methamphetamines d.A sedentary patient who has elevated homocysteine levels

Answer: B Rationale: Her low platetetcount is significant and warrants further investigation.The hemoglobin is low but not at a critical level. The WBC and RBC counts are within the normal range.

The nurse practitioner orders blood work for B.C. While reviewing the results of her complete blood count (CBC), which finding would be of greatest concern to the nurse? a.Hemoglobin of 11.4 g/dL b.Platelet count of 80,000/μL c.White cell count of 4500/μL d.Red cell count of 4.5 ×10 6/μL

Answer: B Rationale: Patients should be taught to exercise to the point of discomfort, stop and rest, and then resume walking until the discomfort recurs. Smoking cessationand proper foot care are also important interventions for patients with peripheral arterial disease.

The nurse teaches a patient with peripheral arterial disease. The nurse determines that further teaching is needed if the patient makes which statement? a."I should not use heating pads to warm my feet." b."I should cut back on my walks if it causes pain in my legs." c."I will examine my feet every day for any sores or red areas." d."I can quit smoking if I use nicotine gum and a support group."

Answer: B Rationale: An elevated blood pressure and cigarette smoking (causes vasoconstriction) increase the rate of atherosclerosis. Atherosclerosis increases the workload of the heart and increases myocardial oxygen demand.

Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are a.Obesity and smokeless tobacco use. b.Hypertension and cigarette smoking. c.Elevated serum lipids and diabetes mellitus. d.Physical inactivity and elevated homocysteine levels.

Acute Coronary Syndrome ACS

When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops. *Results if chronic stable angina worsens*. Falls under the umbrella of CAD. When patients first present with chest pain, ST-elevations on the 12-lead ECG are most likely indicative of a STEMI. •ACS is caused by the decline of a once stable atherosclerotic plaque. The previously stable plaque ruptures, releasing substances into the vessel. This stimulates platelet aggregation and thrombus formation. •Result: Partial occlusion of coronary artery: UA (Unstable Angina) or NSTEMI Total occlusion of coronary artery: STEMI CLINICAL MANIFESTATIONS: *UNSTABLE ANGINA:* •New in onset, unpredictable. •Occurs at rest •Increase in frequency, duration, or with less effort •Pain lasting > 10 minutes •Needs immediate treatment •Symptoms in women often under-recognized: These include fatigue, shortness of breath, indigestion, and anxiety. *Fatigue is the most prominent symptom.* CLINICAL MANIFESTATIONS: *MI:* •Result of abrupt stoppage of blood flow through a coronary artery, causing irreversible myocardial cell death (necrosis) Occur in setting of Preexisting CAD - *STEMI - occlusive thrombus = ST elevation* "A STEMI is an emergency situation. In order to limit the infarct size, the artery must be opened within 90 minutes of presentation. This can be done either by PCI or *thrombolytic (fibrinolytic) therapy*. PCI is the first line treatment if a hospital is capable of performing PCI" PCI goal is to open block arteries with cardiac Cath; local anesthesia. "Reperfusion therapy includes emergent PCI (preferred) or thrombolytic therapy for STEMI. The goal in the treatment of STEMI is to save as much heart muscle as possible. Dual antiplatelet therapy and heparin are also used" - *NSTEMI - non-occlusive thrombus = non-ST elevation* Not as emergency. Cath within 72 hours. Thrombolytic therapy not needed. "For patients with UA and NSTEMI, aspirin and heparin (UH or LMWH) are recommended. Dual antiplatelet therapy (e.g., aspirin and clopidogrel) and heparin are recommended for NSTEMI patients." •*Pain = hallmark of MI* Severe chest pain not relieved by rest, position change, or nitrate administration •Heaviness, pressure, tightness, burning, constriction, crushing •Substernal or epigastric •May radiate to neck, lower jaw, arms, back Often occurs in early morning Atypical in women, elderly No pain if cardiac neuropathy (diabetes) •Catecholamine release and stimulation of SNS Release of glycogen Diaphoresis Increased HR and BP Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch •Cardiovascular Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) Crackles Jugular venous distention Abnormal heart sounds •S3 or S4 •New murmur •Nausea and vomiting Reflex stimulation of the vomiting center by severe pain Vasovagal reflex •Fever Up to 100.4° F (38° C) in first 24-48 hours Systemic inflammatory process caused by heart cell death COMPLICATIONS: MI: •Dysrhythmias: V-fib, V-tachycardia •Heart failure: Left-sided HF •Mild dyspnea, restlessness, agitation, slight tachycardia initially, pulmonary congestion. Right-sided HF: •Jugular venous distention, hepatic congestion, lower extremity edema •Cardiogenic shock •Dressler syndrome: "Dressler syndrome is pericarditis and fever that develop 1 to 8 weeks after MI" DIAGNOSTIC STUDIES: UNSTABLE ANGINA AND MI: •Detailed health history •12-lead ECG Compare to previous ECG Changes in QRS complex, ST segment, and T wave Distinguish between STEMI and NSTEMI Serial ECGs reflect evolution of MI Cardiac Biomarkers: troponin and CK •Coronary angiography: For patients with a STEMI have to go under within 90 minutes Not for patients with UA or NSTEMI •Pharmacologic stress testing For patients with abnormal but nondiagnostic ECG and negative biomarkers CARE: •Initial interventions 12-lead ECG Upright position Oxygen - keep O2 sat > 93% IV access Nitroglycerin (SL) and ASA (chewable) Statin Morphine •Thrombolytic therapy: Only for patients with a STEMI •Agencies that do not have cardiac catheterization resources Given IV within 30 minutes of arrival to the ED Patient selection critical DRUG THERAPY: ACS IV nitroglycerin (NTG) Morphine β-adrenergic blockers ACE inhibitors Antidysrhythmicdrugs Lipid-lowering drugs Stool softeners CARE: •Nutritional therapy Initially NPO Progress to •Low salt •Low saturated fat •Low cholesterol

Answer: a Rationale: History of a close blood relative (e.g., father to son) with hypertension is associated with an increased risk for developing hypertension; atherosclerosis is the most common cause of cerebrovascular disease. Hypertension is the major risk factor for cerebral atherosclerosis and stroke.

While performing blood pressure screening at a health fair, the nurse counsels which person as having the greatestrisk for developing hypertension? a.A 56-year-old man whose father died at age 62 from a stroke b.A 30-year-old female advertising agent who is unmarried and lives alone c.A 68-year-old man who uses herbal remedies to treat his enlarged prostate gland d.A 43-year-old man who travels extensively with his job and exercises only on weekends

Chronic Heart Failure

§Dependent on age, underlying type and extent of heart disease, and which ventricle is affected §*FACES*: §Fatigue §Limitation of Activities §Chest congestion/cough §Edema §Shortness of breath CLINICAL MANIFESTATIONS: §Fatigue §Dyspnea §Orthopnea §Paroxysmal nocturnal dyspnea §Tachycardia Edema: §Dependent, liver, abdominal cavity, lungs §Pitting Edema §Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF §Nocturia §Skin changes = swelling §Behavioral changes = restlessness, confusion §Chest pain §Weight changes = fluid retention DRUG THERAPY: *Diuretics:* §Reduce edema, pulmonary venous pressure, and preload §Promote sodium and water excretion §Loop diuretics §Thiazide diuretics §Monitor potassium levels (hypokalemia) *RAAS inhibitors:* §ACE inhibitors §ARBS §Aldosterone antagonists: Spironolcatone §Monitor potassium levels (hyperkalemia) *β-Blockers* V*asodilators*: §Nitrates Combination therapy: §*BiDil:* hydralazine and isosorbidedinitrate(Bidil) may be helpful in African American patients with HF who are gettingoptimal therapy with ACE inhibitors and β-blockers Positive inotropic agents: §*Digitalis (digoxin)* increase the force of cardiac contraction Monitor for hypokalemia with digoxin & loop, thiazide diuretics "Monitor for signs of hypokalemia and hyperkalemia, since these can increase or decrease the effects of digoxin, respectively. •Monitor for early signs of toxicity: anorexia, nausea and vomiting, fatigue, headache, depression, visual changes." Inhibitor of cardiac sinus node: §*Ivabradine(Corlanor)* §Must be in sinus rhythm with resting HR of >70 bpm and taking highest dose β-blockers > Inhibits sinus node > Reduces HR > Decreases risk of hospitalization for worsening HF The most common side effects of ivabradine include symptomatic bradycardia, high BP, atrial fibrillation, and vision disturbance (i.e., flashes of light). NUTRITION: low sodium, low saturated fat, no added salt, small frequent meals. fluid restriction is NOTTTTT REQUIRED Daily weight is important DASH DIET TEACH: s/s of hypo/hyperkalemia BP monitoring Cardiac rehab avoid heat and cold extremes rest after exertion FACES

Assessment of Cardiovascular System

§Murmurs: §Graded on a six-point Roman numeral scale of loudness and recorded as a ratio §Pericardial friction rubs: §Pericarditis: §Inflamed surfaces of the pericardium move against each other §High-pitched, scratchy sounds §May be intermittent and last days to hours

Anemia Caused by Blood Loss: Acute and Chronic

•*ACUTE blood loss occurs as a result of sudden hemorrhage* •*Sources of CHRONIC blood loss are similar to those of iron-deficiency anemia* ACUTE BLOOD LOSS: Causes of sudden hemorrhage: •Trauma •Complications of surgery Conditions or diseases that disrupt vascular integrity: > Hypovolemic shock > Compensatory: increased plasma volume with diminished O2 -carrying RBCs CLINICAL MANIFESTATIONS: •Caused by body's attempts to maintain adequate blood volume and meet oxygen requirements •Clinical signs and symptoms are more important than laboratory values *Pain:* •Internal hemorrhage: > Tissue distention, organ displacement, nerve compression •Retroperitoneal bleeding > *Numbness* > Pain in lower extremities •*Shock is major complication* DIAGNOSTIC STUDIES: •*With sudden blood volume loss, values may seem normal or high for 2 to 3 days* •Once plasma volume is replaced, low RBC concentrations become evident •Low RBC, Hgb, and Hctlevels show up and reflect actual blood loss CARE: •Replacing blood volume to prevent shock: *blood transfusions (packed RBCs) may be needed if the blood loss is significant.* •Identifying source of hemorrhage and stopping blood loss •Correcting RBC loss •Providing supplemental iron Postoperative patients: •Monitor blood loss •Administer blood products for anemia •No need for long-term treatment CHRONIC BLOOD LOSS: Sources of chronic blood loss: •Bleeding ulcer •Hemorrhoids •Menstrual and postmenopausal blood loss •The sources of chronic blood loss are similar to those of iron-deficiency anemia. Management involves: •Identifying the source •Stopping the bleeding •Providing supplemental iron as needed •*The effects of chronic blood loss usually are related to the depletion of iron storage and are considered as iron-deficiency anemia.*

Lymphoma

•*Malignant neoplasms originating in bone marrow and lymphatic structures* •Result in proliferation of lymphocytes •*Two major types* •Hodgkin's lymphoma •Non-Hodgkin's lymphoma (NHL) Hodgkin's lymphoma: Malignant condition with: •Proliferation of abnormal giant, multinucleated cells •*Reed-Sternberg cells* •Located in lymph nodes •Bimodal age-specific incidence •15 to 30 years of age •>55 years of age •Twice as prevalent in males as in females CAUSES: •Cause remains unknown Key factors: •*Infection with Epstein-Barr virus* •*Genetic predisposition* •Exposure to occupational toxins CLINICIAL MANIFESTATIONS: •*Enlargement of cervical, axillary, or inguinal lymph nodes* •*Second most common location is a mediastinal node mass*: •Cough •Dyspnea •Stridor •Dysphagia •*Nodes remain movable and nontender* •*Painless unless nodes exert pressure on adjacent nerves* May experience: •Weight loss •Fatigue and weakness •Fever and chills •Tachycardia •Night sweats •Alcohol-induced pain •Generalized pruritus without lesions •Initial symptoms correlate with a worse prognosis: •Called B symptoms: •Fever > 100.4 F •Drenching night sweats •Weight loss exceeding 10% in 6 months DIAGNOSTIC STUDIES: •Peripheral blood analysis •Excisional lymph node biopsy •Bone marrow examination •Radiologic evaluation CARE: chemotherapy radiation •Therapy must be aggressive •Potentially life-threatening problems are encountered in an attempt to achieve remission •*Secondary cancers:* •*Occur 10 years after treatment for Hodgkin's lymphoma* •Most common secondary malignancies: •Lung cancer •Breast cancer *Non-Hodgkin's Lymphoma (NHL):* •Heterogeneous group of malignant neoplasms of immune system affecting all ages •Primarily B-, T-, or NK- cell origin CAUSE: •Unknown cause •May result from •Chromosomal translocations •Infections •Environmental factors •Immunodeficiency states •Received chemotherapy or radiation •No hallmark feature CLINICAL MANIFESTATIONS: •*Can originate outside lymph node* •Spread can be unpredictable •*Painless lymph node enlargement = Primary clinical manifestation* Patients with high-grade lymphomas: •> Lymphadenopathy •> B symptoms: •Fever •Night sweats •Weight loss DIAGNOSTIC STUDIES: •Similar to Hodgkin's lymphoma: •Lymph node biopsy •*Prognosis for NHL generally is not as good as that for Hodgkin's lymphoma* CARE: Treatment: •Chemotherapy •Radiation therapy •More aggressive lymphomas are more responsive to treatment = More likely to be cured •Hematopoietic stem cell transplant *Rituximab (Rituxan):* > Monitor for symptoms of severe hypersensitivity infusion reactions (Especially with first infusion) •Ibritumomab tiuxetan (Zevalin) •Complete remission is uncommon

Thalassemia

•A group of diseases involving inadequate production of normal Hgb •Results in decreased erythrocyte production •Problem with globulin protein •Abnormal Hgb synthesis •Hemolysis occurs •Autosomal recessive genetic basis (Genetic LINK) *One thalassemic gene = Thalassemia minor (Acute)* •*Two thalassemic genes = Thalassemia major (Chronic)* Thalassemia minor: •Frequently asymptomatic •Moderate anemia •Microcytosis (small cells) •Hypochromia (pale cells) •*Body adapts to reduction of Hgb- thus no treatment is indicated* Thalassemia major: •Life-threatening •*Physical and mental growth often retarded* •Pale and jaundiced •Splenomegaly, hepatomegaly, and cardiomyopathy •Symptoms develop in childhood CLINICAL MANIFESTATIONS: MAJOR •Chronic bone marrow hyperplasia •Hepatitis C CARE: •No specific drug or diet is effective in treating thalassemia Thalassemia major: •*Blood transfusions (keep HGB at 10) or exchange transfusions with chelating agents that bind to iron to reduce iron overloading (Exjade, Deferiprone [Ferriprox], IV or subQ deferoxamine [Desferal]).* With Chelation therapy: Zinc supplements. Ascorbic acid may be needed as it increases urine excretion of iron •*Iron supplements should not be given!!!!* •Splenectomy

Assessment of Hematologic SYstem

•Health History Genetic Risk Alert: •Hematologic problems with a strong genetic link include •Sickle cell anemia, hemophilia, thalassemia, and hemochromatosis •Predispose a person for development of these same issues leukemia, pernicious anemia, and clotting disorders ASSESS: Elimination Pattern: •Bleeding is significant •Hemarthrosis (blood in a joint) occurs in the patient with bleeding disorders and can be painful. Arthralgia (joint pain) may indicate an autoimmune disorder, such as rheumatoid arthritis, or may be caused by gout secondary to increased uric acid production as a result of a hematologic malignancy or hemolytic anemia. •Military history: dioxin-containing defoliant (Agent Orange) in Vietnam War. •Menstrual history, impotence, or high-risk sexual behaviors •Conflicts with transfusions or transplants PHYSICAL EXAM: Skin assessment: •Systematic head-to-toe order •Petechiae •Ecchymoses = brusing •Spider nevus Can indicate bleeding disorders DIAGNOSTIC STUDIES: Laboratory Studies: •Complete blood count > RBCs, WBCs, and platelets >> •Total RBC count alone not always diagnostic •Hemoglobin value (Hgb) •Hematocrit value (Hct) = % of RBC compared with total blood volume; usually 3x's the HGB level. *Decreased RBC = anemia, hemorrhage, hemodiluation (fluid volume excess)* *Increased RBC = dehydration* >> •White blood cells = 4,000 - 11,000 •Total WBC count •*WBC > 11,000/µL is associated with infection*, inflammation, tissue injury or death, and malignancies •*Leukopenia is associated with WBC < 4000/µL = bone marrow suppression, severe/ chronic illness* >> •Neutropenia is a condition in which the absolute neutrophil count (ANC) is less than 1000 cells/µL. •Neutropenia results from a number of disease processes, such as leukemia, or from bone marrow depression, and is associated with a high risk of infection and death from sepsis. >> •Platelet count = 150,000 - 400,000 •Number of platelets/µL of blood *Thrombocytopenia: below 100,000* •*Danger of spontaneous hemorrhage/ bleeding when below 10,000* Thrombocytosis: •Danger of excessive clotting Peripheral smear: •Morphology of blood cells *Pancytopenia:* •Suppression of all blood cells (RBC, WBCs, and platelets) Blood Types Iron metabolism Radiologic Studies: •Computed tomography (CT) •Magnetic resonance imaging (MRI) Biopsies: •Fluorescent in situ hybridization (FISH) •Bone marrow examination •Lymph node biopsy

Iron-Deficiency Anemia

•Most common nutritional disorder in the world Most susceptible: •Very young •Poor diet •Women in reproductive years CAUSES: •Inadequate dietary intake •Malabsorption Blood loss: •2 mL whole blood contain 1 mg iron •Major cause of iron deficiency in adults •Chronic blood loss most commonly through GI and GU systems •Hemolysis: dialysis treatment •Pregnancy CLINICAL MANIFESTATIONS: •Pallor is most common •Glossitisis second = Inflammation of tongue •Cheilitisis = Inflammation of lips DIAGNOSTIC STUDIES: Laboratory findings: •Hgb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets •Stool occult blood test •Endoscopy •Colonoscopy A bone marrow biopsy if other tests are inclusive CARE: •Treat underlying disease causing reduced intake or absorption of iron Replace iron: •Nutritional therapy •Oral iron supplements •Transfusion of packed RBCs (if from acute blood loss) DRUG THERAPY: Oral iron: •Enteric-coated or sustained-release capsules are counterproductive •Daily dose is 150 to 200 mg •Best absorbed as ferrous sulfate in an acidic environment; 1 hour before meals; with Vitamin C or OJ. •Liquid iron should be diluted and ingested through a straw because it stains teeth. Side effects: •Heartburn, constipation (stool softners needed), diarrhea, black stools Parenteral iron (INFeD): known for anaphylaxis; test first. •Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance •Can be given IM or IV IM may stain skin: •Z-track TEACH: Foods high in iron Reassess HGB and RBC to evaluate effectivness •Iron therapy for 2 to 3 months after Hgb levels return to normal •Patients who require lifelong iron supplementation should be monitored for potential liver problems related to iron storage