medsurg hematology – Flashcards
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hematology
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study of blood, blood-forming organs, blood-related disorders
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hematologic system structures
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blood blood-forming organs (bone marrow, spleen, lymph system)
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bone marrow
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hematopoiesis: blood cell production produce non-differentiated immature blood cells (stem cells) - produced in bone marrow and then differentiates into different types of cells (RBC, PLATELET, WBC). if immature blood cells in blood, not in MARROW = problem -blasts CBC w/differential - includes WBCs also
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**TEST ?** immature cells should not be in blood (-BLAST CELLS) (megablast)
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blood cell disorder
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blood
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connective tissue total amount 5 L (average adult)
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three primary functions of blood
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transportation: transport oxygen, nutrients, hormones, waste products throughout the body system Regulation: fluid, electrolytes, acid-base balance protection: combat infection and stop bleeding
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blood components
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plasma & cells
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plasma 55%
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straw- colored liquid component mostly water contains dissolved proteins - glucose, clotting factors, mineral ions, hormones, carbon dioxide
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tissue hypoxia
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less hemoglobin, less RBC
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red blood cells (RBCs) erythrocytes: 45%
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flexible cell, thin membrane Male: 4.3-5.7 million/microliter female: 3.8-5.1 million/microliter lifestpan: about 120 days needs essential nutrietns to make RBCs: protein, iron, folic acid, cobalamin (B12), riboflavin (B2), pyridoxine (B6), thyroid hormone made of hemoglobin molecules to carry oxygen to the body
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white blood cells: leukocytes
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4000-11000/microliter part of the body's immune system help fight infections and diseases
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platelets: thrombocytes
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initiate blood coagulation process in response to injury play roler in the process of clot shrinking and retraction 150,000-400,000/microliter lifespan 5-9 days
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hemostasis
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normal blood clotting mechanisms to minimize blood loss after injury
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four components of hemostasis
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1.vascular response: immediate local vasoconstriction of injured blood vessel (lasts 20-30min. 2. platelet plug formation & aggregation from reaction of the plasma clotting factor 3. form fibrin clots on the platelet plug 4. lysis of clot: fibrinolysis & anticoagulation mechanisms keep the blood to its fluid state
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spleen
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located upper left quadrant functions:: hematopoietic: RBC production during fetal development. Filtration: old & defected RBCs by mononuclear phagocyte system. Bacteria (gram-positive cocci) Immunologic: supply lymphocytes, monocytes, stored immunoglobulins Storage: stored RBCs & platelets (30%) injured spleen = heavy duty hemorrhage
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lymph system
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consists of lymph fluid, lymphatic capillaries, ducts, lymph nodes. lymph fluid: pale yellow, interstitial fluid - too much lymph fluid leads to lymphedema functions:: removal of interstitial fluid from tissue, absorbs and transports fatty acids, transport immune cells to and from lymph nodes
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liver
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filter produces pro-coagulants essential for homeostasis & blood coagulation stores excess iron produces hepcidigin to regulate iron balance
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aging & hematologic system
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dec number of stem cells dec ability to compensate with illness dec Hb levels due to iron deficiency Inc fragility of RBCs dec bone marrow reserve of granulocytes: minimal increase of WBCs with infection
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assessment of hematologic system: subjective data
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PMH, medications, surgeries or other treatments functional health patterns (Table 30-6)
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assessment of hematologic system: objective data
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petechiae: small, purple-red pinpoint regions, ecchymoses: brusising spider nevus spenomegaly hepatomegaly
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assessment of hematologic system: diagnostic studies
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Hemoglobin - gas carrying capacity (female 11-16) (Male 13-17) hematocrit- packed RBC volume - 35%-50% of total vlood volume RBC morphology - shape & size of RBCs - no variation WBC number of leukocytes 4,000-11,000 microliter platelet - number of platelets - 150,000-400,000 microliter
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bone marrow aspiration & biopsy
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outpt procedure, lies on back or side, gets local anesthetic agents, feels pressure, a few seconds of sharp pain during aspiration, local anesthesia <1hr procedure not the same thing as bone marrow harvesting - bone marrow transpant - general anesthesia, surgery 7-8 hr
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post-procedural care of bone marrow aspiration pt
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pressure dressing on site, monitor VS, monitor for bleeding, lie on aspirated site for 30-60min for maintaining pressure on site. allow doing light activity. tylenol PRN
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RBC function
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transport oxygen (O2) from lungs to systemic tissues, carry carbon dioxide from the tissues to the lungs. each RBC contains several hundred thousand hemoglobin molecules which transport oxygen, oxygen binds to heme on the hemoglobin molecule. (PULSE OX) oxygen comes from lungs, attaches to hemoglobin molecules, then released in the tissue cells
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Anemia
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not a specific disease mainifestation of a pathologic process deficiency of: # of RBCs, quantity of hemoglobin, volume of packed RBCs w/in total blood volume (hematocrit)
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risk factors of anemia
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dec. RBC production:: deficient nutrients (iron, folic acid, cobalbumin), decreased erythopoeitin, decreased iron availability. Blood loss:: chronic hemorrhage, bleeding duodenal ulcer, colorectal cancer, liver disease, acute trauma, ruptured aortic aneurysm, GI bleeding inc RBC destruction:: hemolysis, sickle cell disease, medication, incompatible blood, trauma (cardiopulmonary bypass)
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clinical manifestations of anemia
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presented by the bodys response to tissue hypoxia. Hb levels determine severity of anemia: symptoms: yellowing eyes. paleness, coldness, yellowing skin. SOB. muscular weakness. changes in stool color. fatigue, dizziness, fainting. low BP, paliptations, rapid heart rate, chest pain, angina, heart attack. spenomegaly.
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medical/nursing managements of anemia
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dietary and lifestyle changes, blood or blood product transfusions, drug therapy, oxygen therapy. patient teaching: nutrition intake, compliance with drug therapy.
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iron deficiency anemia
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one of the most common form of anemia iron: synthesizing hemoglobin & RBCs lack of iron: make fewer RBCs or small RBC size iron deficiency anemia: low volume of stored iron
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iron deficiency anemia
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transferrin (transports iron) w/o transferrin, iron cannot be out in circulatory system. ferritin (stores iron in liver & heart) iron should not be excreted (not found in stool/urine)
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risk factors of iron deficiency anemia
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inadequate dietary intake: older adults, socioeconomic status malabsorption: GI surgery blood loss: major cause in adult - 2ml of blood = 1mg iron loss. (most common is female mestural cycle). premenopausal women. persons with hemorrhage. chronic renal failure (dialysis.)
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clinical manifestations of iron deficiency anemia
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general manifestations of anemia lack of iron in tissues pallor: most common symptom glossitis: second msot common cheilits: inflammation of the lip
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diagnostic studies of iron deficiency anemia
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history & physical exam, lab findings dec Hb & Hct, dec serum iron (50-175), dec ferritin: amount of stored iron in body (10-250). Inc TIBC & transferrin (250-425) transferrin: main protein in the blood binding to iron to transport it throughout the body. TIBC: measuring amoutn of available transferrin (total iron binding capacity). fecal occult blood test (FOBT): detect iron deficiency due to GI bleeding endoscopy, colonoscopy bone marrow biopsy
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medical management of iron deficiency anemia
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treat the underlying cause increased iron intake
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drug therapy for iron deficiency anemia
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oral iron: first choice: inexpensive, convenient, absorbed from duodenum & proximal jejunum, enteric-coated or sustained-release capsules release iron farther down the GI tract. Best absorbed as ferrous sulfate in acidic environment TAKE ONE HOUR B4 MEALS: most acidic duodenum mucosa. gastric side effect (heartburn) may require iron to take with meals take vitamin C or OJ to inc iron absorption dilute liquid iron to take through a straw to prevent teeth staining, causes stools to become black: GI tract excretes excess iron. side effects: heartburn, constipation, diarrhea
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parenteral iron
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IM injection use Ztrack injection technique 2 separate needle for preparation and injection IV preparation: risk for allergic reaction
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nursing managements (iron deficiency anemia)
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assess Hb & RBC counts: evaluate the effectiveness of treatment emphasize the importance of compliance with dietary and drug therapy: need to take iron therapy for 2-3 months after the Hb level returns to normal to replenish the body's iron storage. monitor for potential liver problem for life-long iron supplement therapy: excess storage too much iron in the liver could cause hepatitis.
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Megaloblastic anemias
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group of disorders caused by impaired DNA synthesis characterized by the presence of large RBCs megaloblastics: macrocytic & abnormal RBCs results from cobalamin & folate deficiency
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cobalamin (vit B12) deficiency
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intrinsic factor (IF): protein secreted by the parietal cells of the gastric mucosa Required IF for cobalmin (B12) absorption in the small intestine
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risk factors (B12 anemia)
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pernicious anemia: inability of producing IF by gastric mucosa GI surgery: lost IF-secreting gastric mucosal cells, impaired absorption of Cobalamin in distal ileum long term use of H2 histamine receptor blockers chronic alcoholism
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clinical manifestations (B12 anemia)
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insidious onset: takes several months for symptom presentation, general symptoms of anemia GI manifestations: sore, red, beefy, shiny tongue. anorexia, N/V, abdominal pain neuromuscular mainifestations: weakness paresthesia of the feet & hands (tingling sensation) dec vibratory & position senses. ataxia (unsteady gait), muscle weakeness, impaired thought process
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diagnostic studies (B12 anemia)
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RBCs appear large and abnormal shapes dec cobalamin level: 200-835 pg/ml normal folate level 3-25 mg/ml schilling test: check cobalamin absorption, evaluate for pernicious anemia, collect 24hr urine specimen. preparation: NPO except water for 8hr before the test. no B12 IM injections w/in 3 days b4 test normal: 8-40% of radioactive vit B12 within 24hours 60% = not being absorbed
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medical management (no intact GI absorption)
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not correct the anemia by increased dietary cobalmin intake. emphasize adequate dietary intake for maintaining good nutrition parenteral administration of cobalamin (IM injection) intranasal cobalamin
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medical management (intact GI absorption)
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may take high-dose oral and sublingual cobalamin. can reverse anemia by providing supplemental cobalamin
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folic acid (folate) deficiency
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required folic acid for DNA synthesis > RBC formation & maturation
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risk factors (folic acid deficiency)
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poor nutrition, anorexia malasorption syndromes drugs, alcohol abuse, hemodialysis
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clinical manifestations (folic acid deficiency)
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insidious onset absense of neurologic problems smooth, red, beefy tongue low folate level: 3-25 mg/ml normal cobalamin level
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managements (folic acid deficiency)
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replacement therapy: folic acid 1 mg daily encourage to eat foods with large amounts of folic acid (green leafy veggies, liver, fish, whole grains) all necessary care for anemia
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aplastic anemia
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pancytopenia: decreased all blood cell types hypocellular bone marrow congenital (chormosomal alterations) - fanconi syndrome, congenitial dyskeratosis, amegakaryocytic thrombocytopenia, schwachman-diamond syndrome aquired - idiopathic/autoimmune, chemical agents and toxins (benzene, insecticides, arsenic, alcohol) drugs (alkylating agents, antiseizure drugs, antimetabolites, antimicrobrials, gold). radiation. viral and bacterial infections (hepatitis, parvovirus)
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clinical manifestations (aplastic anemia)
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manifest abruptly (over days) or insidiously (over weeks-months) symptoms caused by suppression of any or all bone marrow elements general manifestations of anemia (fatigue, dyspnea)
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diagnostic studies (aplastic anemia)
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confirmed by laboratory findings. CBC w/differential dec HB WBC & platelets inc iron level 50-175 mcg/dL (gets kicked out of bone marrow and in circulatory system) inc TIBC (total iron binding capacity) 250-425 mcg/dl bone marrow aspiration: hypocellular with inc fat contents
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medical/nursing managements (aplastic anemia)
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identify and treat the underlying cause prevent complications from infection & hemorrhage poor prognosis for untreated condition: 75% fatal treatment options: bone marrow transplantation, immunosuppressive therapy
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sickle cell disease
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inherited, autosomal recessive disorder characterized by abnormal hemoglobin S (Hb S) in the erythrocyte - stiffen & elongate sickle shape due to low oxygen level. identified during infancy or early childhood incurable disease predominant in african americans 1 in 400 births THESE PTS ARE NEVER PAIN FREE
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types of SCD
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sickle cell anemia ( Hb SS) - most common, severe form, inherit two genes for sickle hemoglobin S sickle cell trait (Hb AS) : SCD carrier, one normal hemoglobin (Hb A) + one sickle hemoglobin (Hb S) Sickle cell thalassemia & sickle cell Hb C disease - inherits Hb S + Hb C genes, less common, less severe than sickle cell anemia
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sickling episodes
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typically asymptomatic except during sickling episodes commonly triggered by low oxygen in the body: de-oxygenation of RBCs or hypoxia Triggering factors: Infection (viral or bacterial) most common trigger. High altitude, stress (physical, emotional), surgery, blood loss, dehydration, acidosis, low body temperature.
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sickle cell crisis
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hospitalized patients severe, painful, acute excerbation of sickling causing vaso-occlusive crisis - impaired blood flow to all body tissues begins suddenly persists for days- weeks; frequency, extent, severity: depending on the % of Hb S present shock: possible life-threatening consequence
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clinical manifestations (sickle cell crisis)
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able to maintain good health have chronic health problem and pain pain: primary symptom: - trivial - excruciating pain prone to cholelithiasis (gallstones) fatigue, jaundice, back pain, breathlessness, arm & leg pain, foot swelling, joint pain
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complications (sickle cell crisis)
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usually fatal by middle age from renal & pulmonary failure prone to infection - pneumonia: most common infection repeated sickling episodes > gradually involve all body organs - spleen, lungs, kidneys, brain: most affected organs due to high O2 needs complications: painful episodes (crises), anemia, organ damage, leg ulcers, bone damage, strokes could cause CIA or TIA depending on where or how severe
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system complications (sickle cell)
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brain - thrombosis or hemorrhage, causing paralysis, sensory deficits or death lung - acute chest syndrome, pulmonary hypertension, pneumonia kidney - hematuria, renal failure bones & joints - hand-foot syndrome, osteonecrosis liver-gallbladder - hepatomegaly, gallstones eye - hemorrhage, retinal detachment, blindness, retinopathy heart - heart failure spleen - splenic atrophy (autosplenectomy) penis - priapism skin - stasis ulcers of hands, ankles and feet
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diagnostic studies (sickle cell)
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peripheral blood smear sickling test electrophoresis of hemoglobin DNA testing
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nursing management
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no specific treatment for SCD goals: alleviate symptoms of disease complications, minimize organ damage O2 for hypoxia and to control sickling pain management: MORPHINE PCA + PRN (BREAKTHROUGH PAIN) ** TEST ?** - must evaluate the effectiveness of opiod analgesics: requires large doses for pain control. demerol contraindicated: high dose leads to accumulation of toxic metabolite IV fluid replacement to prevent dehydration antibiotics blood transfusions in crisis hydroxyurea (Hydrea) - anti-sickling agents stem cell transplant: can cure some patients with SCD
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patient teaching (sickle cell)
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avoid high altitudes frequent rest, maintain adequate fluid intake encourage for vaccination, routine check-ups monitor & seek medical attention with signs of infection
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hemolytic anemia
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RBCs are destroyed & removed from the bloodstream before RBCs normal lifespan of 120days primary RBC destruction site: Spleen third major cause of anemia intrisic factors: defected RBCs: hereditary. abnormal hemoglobin, enzyme deficiencies. RBC membrane abnormalities. Extrensic factors: more common acquired, damaged RBCs by external factors, abnormal immune system reponses (i.e. blood transfusion reaction) blood clots in small blood vessels, certain infections. side effects from medications (i.e. penicillin, indocin, aldomet)
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clinical manifestations/diagnostic studies (hemolytic anemia)
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chills, fever, fatigue, dark urine, rapid heart rate, SOB, splenomgaly & hepatomegaly: hyperactive w/phagocytosis for defective RBCs. jaundice: inc bilirubin level by inc destructed RBCs. coombs test (+)
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medical/nursing managements (hemolytic anemia)
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treat underlying cause, corticosteroids spenectomy administer blood products PRN
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polycythemia - thick blood
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production of increased numbers of RBCs - blood viscosity & volume
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primary polycythemia: polycythemia Vera
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chronic myeloproliferative blood disorder from chromosomal mutation major concern: prone to clotting more common in the elderly (60 yr +) insidiously develops JAK (just another kinase) controlling
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secondary polycythemia
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physical response to body's attempt to compensate for a problem ex: hypoxia - kidney to produce more EPO - inc RBC production tumor produces EPO (i.e. renal cell cancer)
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clinical manifestations (polycythemia)
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HTN: first symptom from hypervolemia & hyperviscosity - headache, vertigo, dizziness, tinnitus, visual disturbances stroke: most common acute complication from thrombosis (BC blood is too thick) Pruritis - excerbated by hot bath erythromelalgia & paresthesia: painful, burning sensation on feet/hands cardiovascular: angina, heart failure, claudication, thrombophlebitis hemorrhagic phenmena - acute & castactrophic hepatomegaly, splenomegaly (90% of pts with polycythemia vera) hyperuricemia - inc RBC destruction
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diagnostic studies (polycythemia)
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inc RBC, WBC (basophilia), platelet counts, Hb, Hct bone marrow aspiration: hypersensitivity
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medical managements (polycythemia)
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goals: reduce blood volume & viscosity & bone marrow activity. phlebotomy: mainstay of treatment. to maintain Hct level <45-48%. remove 300-500 mL of blood every other day until normal Hct hydration therapy: reduce blood viscosity myelosuppressive agents: hydrea, myleran, gleevec, alkeran low-dose asprin: prevent rsik of blood clots agrylin: reduce platelet cout and prevent platelet aggregation analgesics: joint pain anti-pruritic agent antacids: GI disturbances
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nursing managements (polycythemia)
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primary polycythemia - not preventable secondary polycythemia - can be prevented by preventing hypoxia through mainting adequate oxygenation - control chronic pulmonary disease, stop smoking, avoid high altitude. monitor fluid intake & output during hydration therapy active/passive leg exercise & ambulation as possible: prevent thrombus formation by inc circulation on-going treatment: phlebotomy every 2-3 months (500mL each) comfort measures: pain, itching, heartburn emotional support: long-term treatments
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problems of hemostasis - thrombocytopenia
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reduction in platelets below 150,000 mostly acquired condition can be genetic (i.e. wiskott- aldrich syndrome)
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immune thrombocytopenic purpura (ITP)
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autoimmune disease destroyed platelets in the spleen due to not recognized platelets by own immune system platelets lifespan shortened < 8 days.
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thrombotic thrombocytopenic purpura (TTP)
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medical emergency simultaneously occurring bleeding & clotting in ICU, pt usually dies
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heparin-induced thrombocytopenia (HIT)
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platelets gather at the site of an injury to prevent bleeding heparin-induced thrombocytopenia: low platelet counts make it difficult to stop the bleeding
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clinical manifestations (thrombocytopenia)
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generally asymptomatic bleeding (mucosal or cutaneous) first symptom epistaxis (nose bleed), petechiae, purpura, ecchymoses hemorrhage: major complication
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assessment/diagnostic studies (thrombocytopenia)
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history & physical exam platelets < 150,000 thrombocytopenia spontaneous bleeding: platelets < 20,000 bone marrow analysis: may see precoursors of platelets
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medical managements ITP
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immune asymptomatic: not treat until platelets <30,000 corticosteroids: initial treatmetn: solu-medrol IV splenectomy: partial/complete remission IV immunoglovulin immunosuppressive therapy platelet transfusions:: Platelets <10,000 or bleeding before a procedure
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medical management TTP
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thrombotic treat underlying disorder or causative factors corticosteroids plasmapheresis splenectomy immunosuppressive therapy
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medical management HIT
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heparin NO HEPARIN may start coumadin with platelets > 150,000 plasmaphersis protamine sulfate IV thrombin inhibitors: dec coagulation process
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nursing managements thrombocytopenia
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use soft toothbrush don't blow nose hard or pick it monitor signs of occult bleeding no punctures, piercising, invasive treatment use electric razor, no razor blades no aspirin or aspirin-containing products (alka-seltzer, pepto-bismol, herdach remedies) use small gauge needle and apply direct pressure on injection site for 5-10minutes after SQ injection avoid IM injection estimate menstrual blood loss by counting sanitary napkins used during menses: blood loss of 50 mL will completely soak a sanitary napkin properly administer platelet transfusion keep fingernails short
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hemophilia
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X linked (gene located in X chromosome) recessive hereditary bleeding disorder characterized by a deficiency in a blood-clotting factor/protein exclusively in men
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hemophilia A
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factor VIII deficiency: most common form
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hemophilia B
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factor IX deficiency "Christmas disease"
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clinical manifestations (hemophilia)
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slow, persistant bleeding from minor injury/trauma uncontrollable bleeding after dental procedure epitaxis, GI bleeding, hematuria, ecchymosis, hematomas, hemarthrosis
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diagnostic studies (hemophilia)
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normal platelet count inc PTT > 35 seconds: deficiency of intrinsic VIII, IX, XI, XII factor DNA testing, detect carriers of the disease amniocentesis: diagnose hemophilia prenatally
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medical management (hemophilia)
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goal: prevent & treat bleeding major problem: delayed treatment to late or stopping treatment too soon replacement therapy: primary treatment to replace the clotting factor (too low or missing). desmopressin acetate (DDAVP) increase factor VIII levels. may give before surgery, participation in sports, or dental care, prophylactic measures. antifibrinolytic therapy: stabilizing clots in the area. amicar: common drug. gene therapy
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nursing management (hemophilia)
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assess for acute or chronic bleeding (i.e. skin, joints, muscles) check for hematuria & bleeding from the mouth, lips, gums, rectum topical coagulants institute RICE (rest, ice, compression, elevate) manage pain (ibuprofen) no rectal teemperatures PROM exercise: prevent contracture for hemarthrosis avoid weight bearing until swelling resolved medic-alert bracelet padding of furniture corners wear gloves for household chores avoid contact sports use of soft toothbursh & regular dental visits avoid aspirin provide genetic counseling & family support
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WBC disorders: neutropenia
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decrease in circulating neutrophils in the blood normal neutrophil count: 50-70% determine by absolute neutrophil count (ANC) total WBC count x % neutrophil + band forms of neutrophils neutropenia: ANC <1000 severe neutropenia ANC < 500
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risk factors (neutropenia)
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drug-induced: chemotherapy, immunosupressive therapy hematologic disorders autoimmune disorders infections others REVERSE ISOLATION
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clinical manifestations (neutropenia)
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predispose to infection low grade fever + neutropenia: requires immediate intervention. neutropenic fever >100.4 + ANC sepsis
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diagnostic studies (neutropenia)
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history & physical examination WBC with differential counts WBC morphology, Hb & Hct levels reticulocyte & platelet counts bone marrow aspiration cultures (i.e. blood, nose throat, sputum, urine, stool, any lesions) chest x-ray
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medical/nursing management
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identify & remove causative agents antibiotic therapy: Ceptaz, maxipime, primazin, gentamicin, vancomycin avoid rectal temperature & rectal exams administer stool softeners for compinsation strict handwashing and patient hygiene STRICT ISOLATION: private room, positive-pressure/high