hematology alterations (1)

8/4/2019 Hematology Alterations (1)

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19 July 2010Hematologic DisordersMaria Santa Portillo

Caring for Clients with Hematologic Alterations

BLOOD makes 7-10% of the total body weight

female: 4 5 liters male: 5 6 liters

pH: 7.35 7.45 specific gravity: 1.048 1.066 FUNCTIONS:

link to the different organ system

transporter/carrier oxygen and nutrients, CO2 , glucose

controller if you lose blood homeostasis

defender to foreign activities

BLOOD COMPONENTS:

PLASMA liquid part of blood yellow in color

90-91% water, 6-8% proteins, 2% other solutes PROTEINS Albumins

prevents colloidal osmotic pressure big protein molecules remains in the interstitial space regulates blood volume preventing the

occurrence of edema prevents the shifting of water

Serum Globulins Alpha, Beta, Gamma for clotting factors

Fibrinogen, Prothrombin, Plasminogen for clotting factors

CELLULAR COMPONENTS ERTHROCYTES (RBC)

roles (BCC) Buffering power Carry Hmg (hemoglobin)

most important Hmg has carbonic anhydrase (enzyme

that converts CO 2 and H 2O to hydrogenand carbonic acid H2 + CO3)

Catalyzes

characteristics biconcave disk

allow RBC to pass in small vessels easily deformed in any shape lifespan = 120 days

Hematopoeisis: Production of RBCs in utero : liver, spleen, lymph nodes in adult : bone marrow (sternum, ribs,

vertebrae, pelvis)

RBC differentiation:

reticulocytes = body is attempting tocompensate

RBC Regulation: Tissue oxygenation (PPALL)

Poor blood flow Pulmonary disease Anemia Low Hmg Low blood volume

Erythropoietin90% kidney

10% liver* common endpoint = hypoxia ( Olevels in tissues)

RBC Maturation: Folic Acid

sources: green leafy vegetables Vitamin B12

sources: meat ONLY

yolk sac

liver, spleen, and lymph nodes

bone marrow

O2 levels; hypoxemia in blood

hypoxia; O2 in the tissues

kidneys

secrete erythropoietin

hormone acts on bone marrow (stimulated)

facilitate production of RBCs

pluripotent stem cell

proerythroblast (nucleated)

basophil erythroblast

reticulocyte (young RBC)

mature erythrocyte


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Formation of Hemoglobin:

Iron Cycle: absorbs and stored in the duodenum forms of iron in body

4 5grams Fe

65% Hmg 15 30% ferritin (stored iron in liver) 4% myoglobin (muscles) 19% variations heme compounds

needed for intracellular oxidation 0.1% transferrin

after RBC death, Fe is being phagocytizedby the spleen

Fe is being reused

LEUKOCYTES (WBC) fighting for infections mobile units of bodys protective system formed in: bone marrow and lymph tissues function: seek out and destroy types:

Granular (BEN)NORMAL VALUES FUNCTION/FEATURES

BASOPHILS 0 0.7% IgE receptors (during inflammatoryresponse)

HistamineHeparin

EOSINOPHILS 0.5 1% life span = 8 12 daysE(a)limentary and respiratory tractE(a)llergyParasitic infection*asthma = eosinophils

NEUTROPHILS 55 70% first line of defense against bacterialinfection

neutrophils = infection

Non-Granular/Mononuclear Lymphocytes

B lymphocytes humoralimmunity

T lymphocytes thymus, cellularimmunity

Monocytes young macrophages macrophages engulfs

PLATELETS: part of a bigger cell/fragment characteristics:

tiny cell fragments no nucleus formed in bone marrow 150,000 300,000 uL lifespan: approximately 10 days

function plays a role in blood coagulation

**We need 100B new blood cells a day Mechanism of Hemostasis:

orderly, stepwise process for stoppingbleeding that involves:

Vascular phase : vasoconstriction of blood vessels > diameter of bloodvessel > blood volume

Platelet plug formation : aggregation of platelets > collagen stimulatesplatelets > seal off injury

Coagulation : extrinsic and intrinsicfactors

Fibrinolysis or Clot dissolution

ALTERATIONS OF ERYTHROCYTE FUNCTIONS ANEMIA

in Hmg content or red cell mass impairs oxygen transport CLASSIFICATIONS:

based on morphology (cell size and shape) normocytic (normal) microcytic (small) macrocytic (big)

2 important vitamins: Folic acid and Vit B12

required as an essential building block of DNA of RBCs

nuclear maturation and division

protoporphorin IX + Fe ++

heme formation

heme + globin

hemoglobin chain

2 alpha chains + 2 beta chains

Hemoglobin A (HgA) - adult Hmg

vasoconstriction(exposure of collagen)

platelet formation(intrinsic L pathway)

coagulation clotting factor

extrinsic mechanism(tissue thromboplastin)

intrinsic mechanism(blood vessel injury)

prothrombin (common pathway)

thrombin

fibrinogen > fibrin (clot)

activation of clotplasminogen > plasmin


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ETIOLOGY: inadequate RBC production premature or excessive RBC production blood loss (hemorrhage) deficits in nutrients (iron, Vit B12) hereditary factors (sickle) chronic diseases (production of erythropoietin

TYPES: nutritional anemia (inadequate intake)

Iron-deficiency (IDA)

Vitamin B12 deficiency Folic Acid deficiency anemia hemolytic anemia (characteristics)

Sickle cell anemia Thalasemia Glucose-6-phosphate dehydrogenase

bone marrow depression anemia Aplastic anemia

IRON DEFICIENCY ANEMIA NO HMG FORMATION BELOW NORMAL TOTAL BODY IRON INADEQUATE HMG PRODUCTION FOR BODY REQUIREMENTS ETIOLOGY: (5 IS)

I ncrease blood loss I nsufficient dietary Fe intake (doesnt eat green

veggies) I mpaired GIT absorption I ncreased Fe requirements (menstruation,

pregnancy) female: 2mg iron intake additional

I nfection LAB FINDINGS:

microcytic, hypochromic RBC chromic something is wrong with the

Hmg content Hmg lower than hct (hematocrit) serum Fe concentration total Fe binding capacity serum ferritin (because no iron) reticulocyte count (because no iron that can

produce) ASSESSMENT FINDINGS: (FE KAP)

F atigue low O2 capacity in tissues (common)

E xercise Tolerance is decreased K oilonychia

nails become brittle and spoon-shaped(d/t insufficient supply in the periphery)

Angular cheilitis mouth ulcerations, lesions in oral mucosa

P ica, P allor pica feeling of deficiency of something so

you crave (ice, flour, not common) pallor pale

GOALS OF MANAGEMENT: correction of underlying cause treatment through diet and supplemental iron

preparations Vitamin C

SUPPORTIVE MANAGEMENT FOR PATIENTS WITHANEMIA:

meet patient nutritional needs small frequent meals oral lesions soft, cool, bland foods dyspepsia eliminate spicy foods, milk and

dairy products anorexic and irritable give preferred

food, accompany during meals fatigue

adequate rest periods proper scheduling of activities prepare patient for diagnostic testing

schedule all tests to avoid disruptingpatient meal, sleep and visiting hours

finish first light activities before doingheavy ones

prevent complications observe for signs of bleeding monitor transfusions warn patient to change position slowly to

minimize dizziness induced by cerebralhypoxia

set limitations on acts

assess level of tolerance on acts frequent rest periods pace activities

NURSING RESPONSIBILITIES IN FE PREPARATION: assess for use of drugs that can interact with Fe administer with orange juice administer 1 hour AC or 2 hours PC

AC before meals PC after meals

do not give with milk and antacids give with straw

for liquid preparations monitor for Fe toxicity

loss of appetite, fatigue, wt loss, HA,bronze/gray hue to the skin, dizziness,nausea, SOB

monitor Hmg and reticulocyte count stools may be dark green fluids and fibers

to prevent constipation INJECTING IRON SOLUTIONS:

use of z-track technique in the buttocks to prevent staining skin

apply pressure, dont massage watch out for dizziness, HA, thrombophlebitis in

IV site regular check-up and blood studies pinch and twist

MEGALOBLASTIC ANEMIA CHARACTERIZED BY THE PRODUCTION AND PERIPHE

PROLIFERATION OF LARGE, IMMATURE AND DYSFUNCTIONARBCS

MACROCYTIC ANEMIA TYPES:

Vitamin B12 deficiency (Pernicious) anemia Folic Acid deficiency anemia


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SICKLE CELL CRISIS occurs when client experiences O2 resulting

in the enlargement of rigid sickle-shaped cells vaso-occlusive crises/pain crises aplastic crises

infection with human parvovirus hyperhemolytic crises sequestration crises

other organ pool the sickled cells DIAGNOSTICS:

sickle slide preparation (microscopic) sickle-turbidity tube test Hb electrophoresis diagnostic test x-ray abdominal UTZ trancranial dopper UTZ

INTERVENTIONS: acute pain

assess PQRST monitor effectiveness of analgesia monitor I&O

when dehydrated = O2 apply heat to joints as ordered provide rest periods administer fluids oral fluid intake drugs

morphine acetaminophen NSAIDS

other pharmacological management hydroxyurea sodium cromoglycate folic acid supplement Fe supplement blood transfusion penicillin prophylaxis (prevent infection) pneumococcal vaccination (prevent

infection)

readiness for enhanced self-care client education

explain nature of disease adherence to treatment regimen,

follow up routine CBC count genetic counseling

alert young women with sickle cellanemia that pregnancy carries a high-risk for them

explain complications and how toprevent crises

APLASTIC ANEMIA PRIMARY CONDITION OF BONE MARROW STEM CELLS BONE MARROW FAILS TO PRODUCE ALL THREE TYPES OF BLO

CELLS(PANCYTOPENIA ALL BLOOD COMPONENTS ARE LOLEVES)

anemia no RBC infection no WBC bleeding no platelet

ETIOLOGY: 50% idiopathic chemical damage: benzene, arsenic,

chloramphenical, chemo drugs viral infections: mononucleosis, Hep C, HIV exposure to radiation

CLINICAL MANIFESTATIONS: anemia leukopenia

low levels, recurrent/multiple infection thrombocytopenia

petechiae, tendency to bleed excessively MANAGEMENT:

eliminate any identifiable cause explain patient condition educate public about hazards of toxic agents prevent infection prevent bleeding prevent falls continue normal lifestyle with appropriate

restrictions BONE MARROW TRANSPLANT:

3 categories Autologous

from patient Syngeneic

transplant taken from identical twin Allogeneic

transplant from an HLA-matchedsibling or an unrelated HLA-matchingdonor

HLA = human leukocyte antigen; matchrequired to prevent rejection

Steps Conditioning

pre-treatment of bone marrowtransplant recipient with high doses of chemotherapy +/- total bodyirradiation to destroy the malignancy

Bone Marrow Harvesting needle is inserted into pelvis bone marrow is collected from the

donor under general anesthetic, 500-1200ml of bone marrow from pelvis

Processing removal of red cells and to concentrate

the mononuclear cells

exposure to low O2

defective Hmg

sickle cells

fragile and sticky

impede circulation

microinfarcts

tissue hypoxia


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Transplantation processed donor cells are injected into

the recipient where they find their wayto the bone marrow and attach

most critical days: first 100 days (posttransplantation

before transplantation: patient understanding procedure treatment protocol to be used

venous access during transplantation: monitor VS maintain sterility watch out for complications

after implementation: monitor VS administer meds provide good oral care meticulous skin care observe nursing care

Antithymocyte Globulin (ATG): immunosuppressive agent selectively destroys T-

lymphocytes gamma globulin fromrabbits/horses that have beenimmunized against humanthymocytes

indication: aplastic anemia,transplant rejection

WHY T CELLS? they attack thebone marrow

POLYCYTHEMIA erythrocytosis excessive of RBCs

Hct higher than 55% can be primary, secondary, or relative

SECONDARY POLYCYTHEMIA SOMETHING THAT IS NORMAL PHYSIOLOGIC DISEASE OCCURS AS A RESPONSE TO AN ELEVATED ERYTHROPOIETIN

LEVELS COMPENSATORY RESPONSE TO HYPOXIA

RELATIVE POLYCYTHEMIA NOT DUE TO EXCESS RBC PRODUCTION FLUID DEFICIT RBC COUNT IS NORMAL BUT FLUID LOSS INCREASES CELL

CONCENTRATION CORRECTED BY REHYDRATION

PRIMARY POLYCYTHEMIA/POLYCYTHEMIA VERA/ERYTHREMIA (PV)

NO HMG FORMATION BELOW NORMAL TOTAL BODY IRON INADEQUATE HMG PRODUCTION FOR BODY REQUIREMENTS

CLINICAL FEATURES: blood flow

headache dizziness

sensory deficits (vision, hearing) chest pain viscocity

HTN thromboses (major cause of M/M) SOB, especially when lying flat splenomegaly

venous stasis pphletora: ruddy appearance to face,

especially nose clubbing of fingers dusky appearance to lips and mucous

membranes POSSIBLE NURSING DIAGNOSIS:

pain r/t effects of altered blood flow in thedistal extremities

risk for ineffective tissue perfusion r/t sluggishblood flow and risk for thrombosis

NURSING CARE: health teaching

dangers of smoking ( blood viscocity) adequate hydration prevent blood stasis report signs of thrombosis and bleeding monitor hct and blood counts

MANAGEMENT: periodic phlebotomy

removal of certain amount of blood goal:

blood volume make client non-deficient (no RBC

production) special considerations:

before explain procedure watch out for tachycardia,

clamminess, vertigo VS keep patient supine

after watch out for s/sx of iron

deficiency, bleeding advice ambulation oral fluid intake VS monitor blood counts ambulate slowly

gene aberration hemoblastic cell line

excess production of RBC, WBC and platelets

total blood volume, blood viscocity


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LEUKOPENIA conditions in which there are fewer leukocytes than

normal results from Neutropenia or Lymphopenia

NEUTROPENIA ACUTE POTENTIAL BLOOD DYSCRASIA FAILURE TO PRODUCE ADEQUATE NUMBERS OF NEUTROPHILS

(LESS THAN2000/ MM 3) FEMALE> MALE

SUSCEPTIBLE TO BACTERIAL INVASION AND INFECTION CAUSES: production of neutrophils

aplastic anemia d/t meds/toxins metastatic cancer lymphoma leukemia myelodys plastic syndromes chemo radiation therapy

destruction of neutrophils hypersplenism (splenomegaly) medication-induced immunologic disease (SLE) viral disease (ex. infection, hepatitis,

mononucleosis)

bacterial infections CLINICAL MANIFESTATIONS: rapid onset severe fatigue and weakness sore throat buccal and pharyngeal ulcerations abdominal discomfort fever weak and rapid pulse severe chills

MANAGEMENT: removal of causative factor

disease is usually reversed 2-3 weeks after BMT may be required if condition is not

reversed surveillance cultures of blood, throat, sputum,urine, and stool

to monitor infections treatment includes colony-stimulating factors

(CSF) to neutrophil production given after offending agent is eliminated given before serious infection, prognosis is

better broad spectrum antibiotics control of oral and gingival pain

meticulous oral care saline rinses local anesthetic gels and gargles

soft or liquid food until mouth and gum soresare diminished

NURSING DIAGNOSIS: risk for infection ineffective protection

initiate neutropenic precautions bypreventing complications

MANAGEMENT: environment

strict medical asepsis maintain cleanliness

fresh flowers are not allowedinside the room

maintain cleanliness of room isolation precaution

patient wear mask (avoid inhaling

infections) hygiene (meticulous care in terms

of hygiene) check VS most especially

temperature (for presence of fever)

diet of patient not allowed to eat fresh unpeeled

fruits, microbial diet hydration status

IV status presence of phlebitis watch out for signs of

inflammation

ALTERATIONS OF PLATELETS AND CLOTTING FACTORS PLATELETS ANDCLOTTINGFACTORS FOR NORMAL CLOTTING AND LYSIS TO OCCUR:

intact blood vessels adequate platelets sufficient amount of the 12 clotting factors well-controlled fibrinolytic system

DIAGNOSTICS: complete health history physical exam lab tests

most crucial data to pinpoint the cause of hemorrhage

SIGNS AND SYMPTOMS: petechiae

tiny hemorrhagic spots caused by intradermal (ID) or submucosal bleeding

ecchymosis large, blotchy, SQ hemorrhagic areas

hematoma subdermal hemorrhage

hemarthrosis bleeding in the joints

THROMBOCYTOPENIA most common cause of hemorrhagic disorders decrease in circulating platelets (less than 100,000/uL) 4 major reasons why it occurs:

in platelet production platelet lifespan

blood pooling of spleen dilution of the bloodstream

50,000 uL = minor trauma leads to bleeding 10,000 uL = spontaneous bleeding even without trauma TYPES:

Immune/Idiopathic Thrombocytopenic Purpura Thrombotic Thrombocytopenic Purpura Secondary Thrombocytopenic Purpura Disordered Platelet Distribution


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THROMBOTIC THROMBOCYTOPENIC PURPURA CAUSES:

toxins released after bacterial invasion causeswidespread thrombosis

platelet tend to clump together and infiltrate totissues leading to ischemia

SECONDARY THROMBOCYTOPENIA CAUSES:

usually secondary to drugs/meds (thiazides,

aspirin, NSAIDs, Sulfonamides, Tagamet,Lanoxin, Lavix, Heparin, Morphine, Tegretel, Vit C and E)

spices (ginger, garlic) infections (bacterial or viral) bone marrow disorders chemotherapy, radiation therapy

IMMUNE THROMBOCYTOPENIC PURPURA IDIOPATHIC THROMBOCYTOPENIC PURPURA HEMORRHAGIC AUTOIMMUNE DISEASE THAT RESULTS IN

DESTRUCTION OF PLATELETS ETIOLOGY AND RISK FACTORS:

binding of auto-antibodies to antigens on platelet membrane

common among women: 20-40 years old children: after a viral infection onset

PATHOPHYSIOLOGY:

DEADLY DILLEMAS: spontaneous hemorrhage, cerebral, GIT, GUT,

diaphragm nerve pain, extremity anesthesia and paralysis

SIGNS AND SYMPTOMS: (GSHEEEP) Gingival bleeding S plenomegaly (tend to eat foreign platelets) H eavy menses (menorrhagia) E cchymosis E pistaxis E asy bruising P etechiae

DIAGNOSIS: platelet count below 100,000 prolonged bleeding time with normal

coagulation time capillary fragility (+) platelet antibody screening bone marrow aspirate containing normal or

number of megakaryocytes (where plateletscame from)

MEDICAL MANAGEMENT: goal: safe platelet count high-dose corticosteroids

SE: moon-faced, buffalo-hump, susceptibleto stress

suppresses platelet destruction plasmapheresis (short-term therapy) IV gamma globulin ( platelet count) splenectomy

60-80% results in complete/permanent

remission immunosuppressive drugs Vincristine Vinblastine Azathioprine

NURSING MANAGEMENT: health teaching

signs of disease exacerbation side effects of drug being taken by client

(corticosteroids) prevention of bleeding

soft bristle toothbrush electric shavers care with trimming nails

avoid rectal temperature taking, enemasand suppositories

avoid IM injection avoid activities that ICP avoid sexual intercourse if platelet count is


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S pontaneous hematuria H ematoma E pistaxis, bleeding of other mucous membranes P ain

MEDICAL MANAGEMENT: fresh frozen plasma (contain clotting factors) factor VIII and IX concentrates

during acute bleeding, preventive measurewhen undergoing procedures

Aminocaproic acid

fibrinolytic enzyme, slows the dissolution of clots

Desmopressin Vasopressin analog induces transient rise in factor VIII

NURSING MANAGEMENT: applying pressure on minor trauma splinting with joint or muscle hemorrhages avoid injections and all other invasive procedures

perform only after administration of appropriatefactor replacement

analgesics for pain warm bath may improve and lessen pain

during hemorrhagic episodes, rest on

accentuate bleeding cold compress is used

wear necessary medical band for identification during hemorrhagic episodes

careful assessment for emergent complications frequent VS monitoring watch out for: respiratory distress and altered

LOC assist patient in coping and accepting condition health teaching

activity restriction self-care measures safety at home and workplace avoid any agents that interfere with platelet

aggregation (aspirin, NSAIDs, etc) dental hygiene

DISSEMINATEDINTRAVASCULARCOAGULATION(DIC)

complex syndrome of activated coagulation loss of balance between the clotting and lysing system of

the body consumptive coagulopathy DIC starts with excessive clottings

clotting factors depleted excessive bleeding ensues

CATEGORIES OF RISK FACTORS: (STIDS) Secondary response to primary insult Tissue coagulation factors Infection (most common cause)

gram (-) septicemia typhoid fever rocky mountain spotted fever

Damage to vascular endothelium Stagnant blood flow

CONDITIONS THAT MAY PRECIPITATE DIC: shock cirrhosis snake bite glumerulonephritis septicemia retention of a dead fetus trauma heat stroke

PATHOPHYSIOLOGY:

MANIFESTATIONS: classified: acute, subacute, and chronic characterized by widespread bleedings thrombosis bleeding at 3 unrelated sites

DIAGNOSIS: screening assays confirmatory assays ( par tial thromboplastic time) presence of DIC pathology

MANAGEMENT: goals:

identification and correction of precipitatingcause or problem

reestablishing hemostasis by replacing missingblood components (depends on type)

supportive therapy to control manifestation of hemorrhage and thrombosis

control bleeding gabexate and aprotinin

IV heparin administration used to control thrombosis may also cause bleeding to dissolve the clot

NURSING MANAGEMENT: assess all body systems

integumentary respiratory: tachypnea, hemoptysis, orthopnea,

pulmonary infarction cardio: tachycardia and hypotension

GI: abdominal distention, hematemesis (+),guaiac test (test for blood in stool)

GUT: hematuria, oliguria neuro: vision changes, dizziness, HA, changes in

mental status general goals:

monitor and quantify blood loss provide supportive therapy with blood

components resolve manifestations of hemorrhage control further bleeding


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