CHAPTER 37: CARDIOVASCULAR: BLOOD & LYMPH SYSTEMS BLOOD: Heart pumps 5-6 liters of blood per minute Blood plasma consists of o H20, proteins (albumin), electrolytes, lipids, carbohydrates, organic and inorganic substances THE FORMED ELEMENTS IN PLASMA ARE: RBC’s, WBC’s and PLATELETS RBC’S called erythrocytes: 4.5-6.1 million FUNCTION: 1. Oxygenate body tissue 2. In capillary bed of alveoli -blood exchanges 02 and C02 3. Hemoglobin is protein in RBC’s that carries 02 & is responsible for exchange of 02 &C02 4. Hematocrit- 42%-45% (% of RBC’s in blood volume) WBC’S called leukocytes-n 5,000-10,000 Fight infection & assist with immunity (Increase in WBC’s indicates Infection, Inflammation, necrosis or Leukemia Increase in WBC’s is Leukocytosis Decrease in WBC’s is Leukopenia PLATELETS : known as thrombocytes, active in blood clotting Prothrombin & Thromoplasin plus Calcium form= Thrombin Thrombin joins with Fibrinogen to form: Fibrin Fibrin strands form: clot BLOOD TYPES: On the surface of RBC membranes are ANTIGENS if A antigen is on RBC surface ====TYPE A if B is on the surface then it is type B if A+B it is type AB if no antigens then the blood type is O Type AB is known as universal recipients Type O is known as universal donor RH FACTOR: Persons who have D-antigen have RH factor---- they are positive + Have factor means positive Persons who do not have D-antigen lack RH factor----are said to be negative Lack of factor mean--- negative 85% of population and are positive, 15% lack and are negative RH IncompatibilityNegative mom – positive dad- 85% chance baby will be positive At birth Mom with RH- blood is exposed to RH+ blood (baby’s blood is +) Mom will have anti RH- antibodies may cause problems with next pregnancy (erythroblastosis fetalis) mental retardation Mom is given Rhogam to neutralize antibodies BLOOD TRANSFUSION Purpose: 1. To replace blood components because of hemorrhage, anemia, clotting factors or blood deficiencies 2. Before transfusion lab does a cross match 3. Blood should be administered within 30 minutes after being obtained from the lab Procedure: 1. 2. 3. 4. 5. Take baseline vital signs before Give blood 18 gauge (piggyback the blood with .9%NSS ) 2 nurses check blood Start blood slow, 50cc hour Take vital signs- observe for reaction(chest pain, dyspnea, decreased bp, chills, fever (101.4 or higher) 6. No reaction then speed up the rate (50cc-100cc) 7. Take vital signs for one hour 8. Infusion should be complete within 4hour (1 unit is approx 375cc) Autologous Blood Transfusion Patient receives own blood (eliminates possibility of reaction or disease transmission LYMPATHITIC SYSTEM Function: 1. Transports excessive fluid from interstitial spaces to circulatory system 2. Protects body against infectious organisms and also assists with immunity. SYMPHATIC SYSTEM CONSITS OF Lymph fluid & vessels Lymph nodes can be superficial or deep Superficial can be palpated( i.e. neck, groin, axillary) they are easily palpated when infected or swollen CA cells can enter the lymphatic system and escape into circulation or other body tissues such as lungs These CA cells can reproduce and spread to other body parts LYMPH ORGANS Spleen- removes old RBC’s, platelets, and microorganisms from blood during infection it enlarges to release WBC’s to fight infection Thymus: actively involved in immunity, this organ is large in childhood but decreases in size ASSESSMENT OF PATIENT WITH BLOOD DISORDERS: Subjective data: 1. 2. 3. 4. 5. Sex, ethic background and race are important Clients occupation and hobby Military (exposure to toxic chemicals) OTC meds- (ASA) Recent infections, night sweats, bleeding problems, recent transfusions, past surgeries 6. Neurologic symptoms- numbness, tingling, breathing or vision problems 7. G.I. ulcers 8. Alcohol consumption Objective data: 1. 2. 3. 4. 5. 6. 7. Vital signs, increased temp Recent weight gain or loss Lab values Check lymph nodes (freely movable, firm, & nontender) Assess skin for bruises, lesions, brittle nails Urine & stool for OB Dyspnea, enlarged abdominal, swallowen joints COMMON DIAGNOSTIC TESTS: 1. 2. 3. 4. 5. list on pg 779 PPT PT Hgb Hct WBC’s RBC’s DISORDERS: Anemeia manifest with decreased RBC’s and low Hgb Causes: 1. Decreased RBC’s 2. Increase in destruction of RBC’s 3. Blood loss Iron deficiency anemia - body does not have enough FE to synthesize Hgb Causes: 1. Decreased dietary intake 2. Decreased FE absorption 3. Increase demand for FE (ie: pregnancy) Seen most frequently: 1. 2. 3. 4. Premature infants Adolescent girl Alcoholic Elderly S/S: 1. Fatigue 2. Loss of appetite 3. Decreased to concentrate 4. Pallor Chronic anemia S/S: 1. Tachy 2. Exertional dyspnea 3. Hypotension 4. Dysphagia 5. Stomatits 6. Brittle nails DIAGNOSTIC TESTS: 1. 2. 3. 4. 5. Decreased RBC’s Low Hgb Low Hct Low serum FE High FE bending capacity (TIBC) PHARMACOLOGICAL: 1. Oral FE preparations (i.e.Feosol ) (don’t give FEwith milk: Milk decreases FE absorption) 2. Take thru straw- stains teeth 3. Parenteral route of admisinstrion should be given Z track DIET: 1. Foods rich in FE (red meats, raisins, fish, apricots, dark green veggies, dried beans, eggs) 2. Diet high in vitamin C assess vital signs in absorption of FE 3. FE supplements Activity: Frequent Rest Periods APLASTIC ANEMIA- when there is no known cause is known to be congenital: 1. 2. 3. 4. Pancytopenia- def in any of the blood cell elements Decreased RBC’s Decreased WBC’s Decreased platelets SECONDARY APLASTIC ANEMIA Causes: exposure to viruses, chemicals (ie benzene glue), radiation and certain meds, (ie antineoplastics) S/S: 1. Fatigue, weakness, tachy, dyspnea, increased susceptibility to infection, petchial, gingival bleeding and epistaxis DIAGNOSTIC: Bone marrow aspiration MEDICAL MANAGEMENT: 1. Immunosuppressants 2. Transfusion RBC’s and platelets SURGICAL MANAGEMENT: 1. Bone marrow transplant from HLA 2. Immunosuppressant : cyclosporine (sandimmine) to decrease graft rejection Pharmacological 1. Infection treated with antibodies 2. Steroids 3. Androgens PERNICIOUS ANEMIA Autoimmune disease that effects the parietal cells of the gastric mucosa that secretes a protein intrinsic factor that is essential for the proper absorption of vitamin B 12 Without secretion of intrinsic factor vitamin B 12 cannot be absorbed Incidence: 1. Seen most often in patients who have had gastrectomy 2. Female African Americans 3. Patients should be monitored closely for gastric carcinomas Diagnostic Tests 1. Schelleny 2. Gastric analysis S/S 1. Has insidious onset 2. Extreme weakness 3. Sore tongue 4. Numbness and tingling of extremities 5. Edema of legs 6. Atoxia 7. Dizziness 8. Dyspnea 9. H/A 10.Fever 11.Blurred vision 12.Tinnitus 13.Poor memory ect. Pharmacological: 1. Tropical anesthias (oral discomfort) 2. Cyanocobalamin (vit B 12) given IM daily for two weeks then weekly until Hct returns to normal Then monthly for the rest of their lives. VITAMIN B 12- cannot be given orally b/c it cannot be absorbed without the intrinsic factor 3. Folic acid (folate) 4. Diet high in folic acid: green leafy veggies, meat, fish, legumes and whole grains 5. FE is usually not prescribed ACQUIRED HEMOLYTIC ANEMIA: Hemolytic anemias- causes hemolysis or destruction of RBC’s --- release of FE and Hemoglobin Cause: 1. 2. 3. 4. 5. 6. Autoimmune reaction Radiation Blood transfusion Chemicals (lead) Meds (penicillin, methyldopa, gantrisin) A substance produced by bacterium (clostridium) S/S 1. Jaundice 2. Palpatations 3. Hypotension 4. Dyspnea 5. Back and joint pain DIAGNOSIS TESTS 1. Decrease in Hgb and Hct, increase in LDH MEDICAL 1. Remove cause 2. Blood transfusion 3. Erythocylopheresis (a procedure that removes abnormal RBC’s and replace them with healthy RBC’s SURGICAL 1. Splenectomy (will stop destruction of RBC’s b/c spleen is to destroy RBC’s PHARMACOLOGICAL 1. Corticosteroids- decrease autoimmune response 2. Folic Acid- increase in production of RBC’s SICKLE CELL ANEMIA: Genetic disorder which there is abnormal Hgb S rather than Hemoglobin A in the RBC’s Condition occurs most frequently in Africa-American. It also occurs in persons from Asia Minor, India, Mediterranean, and Caribbean areas. SITUATIONS THAT PRECIPATATE SICKLE CELL ANEMIA ARE: 1. 2. 3. 4. 5. Dehydration Fatigue Infection Emotional stress Alcohol consumption When 02 is compromised the RBC’s become sickled. (cresent shaped) obstructed capillaries and larger vessels S/s 1. 2. 3. 4. 5. Fatigue Jaundice Chronic leg ulcers Tachypnea Dyspnea SICKLE CELL CRISIS: fever, pain, blood loss to various organs, (requires immediate intervention) MEDICAL MANAGEMENT: 1. 2. 3. 4. Infections are treated with antibodies Encourage fluids and IV therapy (3-5 liters a day) Skin graft if leg ulcer Genetic counseling PHARMACOLOGICAL: 1. 2. 3. 4. Folic Acid (daily) Cetided citrate (has antisickling effect) Trental PCA pump with morphine POLYCYTHEMEA: 2 TYPES 1. 2. 3. 4. Increase production of RBC’s Usually WBC’s and platelets also increased Occurs in middle age Jewish men Etiology unknown S/s 1. H/A 2. Epistaxis 3. Dizziness 4. Tennitis 5. Blurred vision 6. Fatigue 7. Weakness 8. Prutitis 9. External dyspnea 10. Angina 11.Increase pulse 12.Increase bp 13.Lips become reddish purple 14.Bruise easily 15.Susceptible to thrombic formation 16.Hyperurciema (increase destruction of RBC’s, Hgt>18,Hct >55%) MEDICAL: 1. Phlebotomy-Is the usual Rx. ( removal of blood from vein 350-500cc) qod 2. Radioactive phosphorous 3. Radiation therapy PHARMOCOLOGICAL: 1. Antineoplastic drugs (to decrease bone marrow production) A. Mylean B. Cytoxan C. Mustargen 2. Allopurinol (decrease production of uric acid) 3. Antihistamines (pruituis) DIET: 1. High calorie 2. High protein intake 3. Low NA intake 4. AVOID FE containing foods ACTIVITY 1. Regular periods of rest WHITE BLOOD CELL DISORDERS LEUKEMIA : Is a malignancy of blood-forming tissues in which the bone marrow produces immature WBC’s --- crowding out of other cells in bone marrow, causing decreased production of RBC’s and Platelets--- anemia and bleeding disorders There are 2 classifications (acute and chronic) ACUTE: (2types) 1. AML- acute myelocytic leukemia 2. ALL- acute lymphocytic leukemia CHRONIC: (2types) 1. CMI- chronic myeloctic 2. CLL- chronic lymphocytic leukemia ETIOLOGY of AML 1. There is a connection with survivors of Japanese A bomb and exposure to radiation 2. Rheumatoid Arthritis that are treated with drugs that suppress the immunes system 3. CA treated with cytoxic drugs and radiation S/s of leukemia 1. Persistent infections with fever and chills 2. S/S of anemia 1. Fatigue 2. Pallor 3. Malaise 4. Tachy 5. Tachypnea 3. Bleeding, tenderness, and client will experience bruising, epistaxis, gingival bleeding and increased menstrual bleeding 4. Weight loss, night sweats, swollen lymph nodes 5. H/A visual disturbances 6. Bone pain ACUTE LEUKEMIA (ALL) 1. 2. 3. 4. 5. 6. Usually seen in children between 2 and 6 yrs old Rapid onset If untreated client have median survival time (4-6months) Good prognosis with chemotherapy ( 90% remission) If adults (50-70% remission) High risk of ALL occurs in pts with Down’s syndrome ACUTE MYLOCYTIC LEUKEMIA: 1. Occurs frequently in adolescence and 55+ 2. Median survival time if untreated 2-3 months 3. With chemo 50-70% remission With median survival time 2-3yrs MEDICAL SURGICAL MANAGEMENT : Good handwashing Important MEDICAL DIAGNOSTIC: 1. CBC 2. Bone marrow biopsy 3. Lumbar puncture 4. Xray, MRI, or CTscan SURGICAL: 1. Bone marrow transplants (must have compatible donor) 2. Chemo (high doses) 3. Radiation 1. High doses of chemo and radiation are given prior to transplant to destroy WBC’s and bone marrow cells PHARMACOLOGICAL- antineoplastic drugs: IV or within spinal cord: b/c chemo does not cross blood-brain barrier 1. 2. 3. 4. 5. 6. 7. 8. Oncovin Deltasone Purithol Methotrexate Ditasone Radiation Blood transfusion Antibiotics DIET: Bland, High protein, high carbs Avoid 1. Extreme hot or cold foods 2. Alcohol ACTIVITY Frequent rest periods CHRONIC LEUKEMIA 1. Occurs in adults 50-70 yrs old 2. Higher in men then women 3. Clients Rx with chemo have life expectancy of 2-10 yrs 4. Prognosis depends on severity of disease 5. WBC’s 20,00-100,000 CML- chronic myelocytic leukemia: 1. Occurs in patients 35-50yrs old 2. Higher in men 3. WBC’s 15,000-500,000 MEDICAL DIAGNOSTIC- CBC and Bone marrow biopsy SURGICAL Bone marrow transplant PHARMACOLOGICAL 1. CLL>>>>>Chemo- (Leukaran, cytoxin, oncovin, prednisone) 2. CML>>>>>Chemo- (Myleran, Hydrea, DAT) 3. Interferon- (increases survival time) DIET: High protein, high carbs, high vitamins, bland non-irritating diet. AVOID alcohol ACTIVITY 1. Conserve energy AGRANULOCYTOSIS: Severely reduced # of granulocytes CAUSE: Adverse reaction to meds or med toxicity from: A. Butazolidine, chloromycetin, penicillin, cephalosporins, dilantin, antihistamines, oncovin, prolixin, thorazine and sparine B. Chemo, radiation, bacterial and viral infection S/S 1. H/A- fever, chills, fatigue, ulcerations of mucous membranes of nose, mouth, pharynx, vagina and rectum 2. WBC’s decreased MEDICAL Rx: symptomatic 1. Rx infection 2. Blood cultures PHARMACOLOGICAL 1. Antibiotic DIET: soft, bland, high calorie, high protein, high vitamins ACTIVITY: alter periods of activity with periods of rest COAGULATION DISORDERS: very serious and potentially FATAL disease DIC: Disseminated Intravascular Coagulation: A syndrome that occurs b/c of a primary disease process or condition where there is alternating clotting and hemorrhaging A. B. C. D. E. F. G. H. I. J. K. Burns Acute leukemia Mets CA Polycythemia Pheochromocytoma Shock Acute infection Septic abortion Abruptio placenta Blood transfusion reaction Trauma The condition stimulates the clotting mechanism causing very small clots to form --the body’s fibrinolytic process to stop the clotting—hemorrhage (Small clots block the arterioles and Capillaries…That stimulates the body’s fibrinolytic process that stops the clotting and leads to hemorrhaging) S/S 1. Purpura 2. Bleeding tendencies 3. Renal impairment (decreased output)—renal insufficiency MEDICAL MANAGEMENT 1. 2. 3. 4. Increased PT &PTT and increase Thrombin time Decrease in fibrinogens and platelets Symptomatic: (treat primary condition) Administer whole blood or blood products- platelets and packed red blood cells 5. Cryoprecipitate of fresh- frozen plasma is given PHARMACOLOGICAL: 1. Heparin (Rx. Is controversial) 2. Amicar HEMOPHILIA: Appox: 18,000 people have Inherited bleeding disorder where there is lack of clotting factors The hemophilia tract is carried on the recessive X chromosome (ie mother is asymptomatic-can carry and pass trait to son) 2types Hemophilia A- Lacks clotting factor 8 Hemophilia B- Lacks clotting factor 9 3 classifications 1. Severe: factor level (<1% is normal) 2. Moderate: Factor level (1%-5% is normal) 3. Mild : factor level 40% is normal S/S 1. 2. 3. 4. Severe bleeding with trauma Spontaneous ecchymoses & bleeding from mouth, GI and Urinary tracts Hemarthrosis- bleeding into joints (pain, swelling, redness and fever) Intracranial hemorrhage (most common cause of death) MEDICAL MANAGEMENT 1. Administer clotting factors that pt lacks 2. Administer fresh frozen plasma 3. Keep pt safe (helmet) PHARMACOLOGICAL Desmopressin acelate (DDAVP) to decrease fibrinolytic process THROMBOCYTOPENIA: decrease in # of platelets CAUSE: 1. Aplastic anemia, tumors, leukemia, and chemo 2. Decrease in platelet destruction either drug induced or idiopathic 3. Decrease in platelet survival as in infection or viral disease S/S 1. Petchiae 2. Echymosis 3. 4. 5. 6. Bleeding from mucus membranes Bleeding from internal organs Platelet ct decreased Hgb, hct decreased MEDICAL MANAGEMENT 1. Transfuse platelets 2. Apheresis (removal of unwanted componenets) SURGICAL 1. Spleenectomy Pharmacalogical: Immunosuppressant, gamma globulin and vitamin K DIET: high fiber LYMPH DISORDERS: Lymphatic system 1. Transports excess fluid from interstitial spaces 2. Protects body against infection LYMPHOMA- A tumor of the lymphatic system HODGKINS DISEASE CAUSE: unknown, maybe correlated with mono, associated with virus Epstein Barr INCiDENCE: 1. High in adolescent and young adults S/S 1. Painless swelling in lymph nodes (neck and groin) 2. High temp- night sweats, weight loss DIAGNOTIC: 1. Biopsy (Reed-Sternberg cells isolated) 2. CBC, platelet count, bone marrow aspiration, chest xray, CAT scan, Lymphangiogram MEDICAL MANAGEMENT 1. Stage disease (using staging system to determine progression in body) Chart P. 1138-39 2. Rx: chemo and radiaton SURGICAL: 1. Laparotomy if liver and spleen involved PHARMACOLOGICAL 1. 2. 3. 4. Antiemetic (zofran) during radiation therapy Analgesics for esophagitis Combination of chemos given thru central line Allopurinol (prevent uric acid renal stones) DIET- high caloric, protein, fluid (2500cc a day) ACTIVITY: rest periods NON-HODGKINS LYMPHOMA- cause B is seen as pt ages, T is seen in skin ca 1. More common then hodgkins 2. 5th most common cause of CA in US 3. 5yr survival rate 63%/ 10 yr survival rate = 51% DIAGNOSTIC 1. Lymph node biopsy (no Reed Sternberg cells on biopsy) 2. Stage disease (to determine progression) S/S 1. Enlarged tonsils and adenoids 2. Enlarged lymph nodes (ie groin, axillary and inguinal) 3. Fever, night sweats, weight loss, excessive, tiredness, indigestion, abd pain, loss of appetite, bone pain 4. PHARMACOLOGICAL Rx: various chemo protocols or combination of chemo PLASMA CELL DISORDERS: MULTIPLE MYELOMA- plasma cells in bone marrow become malignant and crowd out normal cell production destroy normal bone tissue – pain—cause is unknown—normal production of antibodies is changed—highly susceptible to infection S/S 1. 2. 3. 4. Bone pain (1st sign) Long bones ache, joints swollen and tender Low grade fever Malaise DIAGNOSTIC: 1. 2. 3. 4. Bone marrow biopsy (shows large # of immature plasma cells) Xrays Bence Jones protein found in urine Hypercalcemia, hyperurcemia, anemia, hypercalciuria MEDICAL MANAGEMENT 1. Symptomatic Rx 2. Radiation and chemo SURGICAL 1. Laminectomy ( if vertebrae collapse) 2. Surgery (if renal calculi) PHARMACOLOGIAL: 1. Steroids 2. Prednisone 3. Antineoplastics: (Cytoxan, Alkeran, Leukeran) DIET: 1. Small frequent meals (6 small) 2. Increased fluid intake (3-4 liters a day) ACTIVITY 1. Keep ambulatory 2. If bedridden turn often