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WBC normal range
5-10
RBC normal range
4.5-5.5
Hgb normal range
12-17.4
Hct normal range
36-52
MCV normal range
84-96
MCH normal range
28-34
MCHC normal range
32-36
Platelet normal range
140-400
RDW normal range
11.5-15.5
MPV normal range
7.4-10.4
Erythrocytes
RBC
-Reticulocyte = immature RBC produced in bone marrow and released into blood prematurely
-Carry hemoglobin to provide O2 to tissues
Leukocytes
WBC
-Protect the body from bacterial invasion
-Neutrophils arrive within 1 hour, then monocytes
Thromboycytes
Platelets
-Not technically cells, circulate freely, activate with vessel wall injury (hemostasis)
-Lifespan 8-11 days
-Aid in coagulation
Health History
-Ethnicity and family history
-Prior episodes of bleeding
-Nutritional/diet history
-OTC medications and supplements/herbal remedies
-Bleeding, clotting, miscarriages
-Fatigue and weakness, dyspnea, SOB
-History of radiation (pelvic) or chemotherapy (damage to lone bone bone marrow where RBC are made
-Hobbies/occupational/military exposure to toxins
-Alcohol consumption
Physical Assessment
skin, oral cavity, lymph nodes, respiratory, cardiovascular, genitourinary, musculoskeletal, abdominal, central nervous system, gynecologic
Megaloblastic anemia risk factors
deficiency in vitamin B12 (cobalamin) or folate (vitamin B9)
-Individuals who follow a strict vegan or vegetarian diet without B12 supplementation, older adults, and pregnant people
Folic acid deficiency risk factors
People with poor diets, high alcohol use, pregnant women
Diagnostics and Therapeutics
-CBC
-Coagulation studies
-Bone marrow aspiration and biopsy (diagnose iron deficiency)
-Splenectomy
-Apheresis (separates blood into its specific parts to remove something, and is then put back into the body once completed
-Therapeutic phlebotomy
what is anemia
decreased erythrocytes
-bottom line issue = decreased oxygen carrying capacity to tissues
development of anemia
the more rapidly anemia develops, the more severe the symptoms
-an otherwise healthy person can often tolerate as much as 50% gradual reduction in Hgb (months) without pronounced symptoms
-rapid loss of as little as 30% (minutes) may cause vascular collapse in the same person
-with gradual onset Hgb of 9-11 usually has no symptoms except dyspnea on exertion and tachypnea
3 classifications of anemia
hypoproliferative, bleeding, hemolytic
hypoproliferative anemia
defective RBC production
-megaloblastic → bone marrow produced abnormally large immature RBC due to impaired DNA synthesis
-decreased erythropoiesis → iron deficiency
-kidney disease
-inflammation
-aplastic → bone marrow fails to make enough RBC and platelets
-cancer/inflammation
bleeding anemia
blood loss
-GI tract, epistaxis, trauma, genitourinary
hemolytic anemia
altered erythropoiesis → could be from sickle cell disease or thalassemia (inherited blood disorder that prevents the body from making enough Hgb)
-G-6-PD deficiency → inherited, lack of G-6-PD enzyme, causing premature breakdown
-Hypersplenism (hemolysis) → spleen destroys RBC too soon
-Drug induced anemia
-Autoimmune anemia
-Mechanical heart valve
symptoms of anemia
-yellowing in eyes
-paleness, coolness, and yellowing of skin (paleness in skin represents blood loss or decreased RBC production; jaundice occurs bc cells are damaged and release pigment making kin and eyes yellow)
-SOB
-muscular weakness
-changed stool color
-fatigue, dizziness, fainting
-low BP, rapid HR, heart palpitations
-chest pain, angina, heart attack
-spleen enlargement
megaloblastic anemia
folate and B12 deficiency
-results in abnormally large erythrocytes which are usually destroyed before they even leave the bone marrow
-diagnosed by serum testing for levels
-B12 is only found in foods of animal origin
-folate is found in green leafy vegetables and liver (folic acid is a supplement, pregnant women take to prepare for increased blood volume)
folic acid deficiency
-Stored as compounds referred to as folates
-Depleted within months when intake is deficient or needs are increased
-Pregnant women (need for increased erythrocyte production)
-Folic acid deficiency in pregnancy women can lead to neural tube defects, such as spina bifida
-Alcohol increases folic acid requirements (patients who use alcohol typically have a diet deficient in folic acid)
B12 deficiency
pernicious (means to cause harm)
-meaning of pernicious anemia = absence of intrinsic factor normally secreted from gastric cells, B12 cannot be absorbed by the ileum
-malabsorption (crohn’s, gastrectomy, ileal resection, bariatric surgery, older populations)
-lack of intrinsic factor (this binds to B12 and takes it to the terminal ileum where it is absorbed, intrinsic factor antibody test)
-inadequate intake in strict vegans with no meat or dairy intake
-certain medications such as histamine blockers or antacids
symptoms of megaloblastic anemia: folate and B12
weakness, listlessness, fatigue, pallor
symptoms of megaloblastic anemia: B12 only
-neurological symptoms (myelin and spinal cord damage) → paresthesia, confusion, lack of proprioception
-pernicious anemia → smooth, sore red tongue
components of a hemogram
MCV, MCH, RDW, and MCHC
MCV
the average size of your RBC’s
MCH
mean cell Hgb
-the average mass of hemoglobin per RBC in a sample of blood
RDW
measure of the range of variation of RBC volume
MCHC
a measure of the concentration of hemoglobin in a given volume of packed RBCs
assessment of megaloblastic anemia
Tongue = beefy red and sore
Corner of mouth ulcerated = angular cheilitis
management of megaloblastic anemia
replace folate or vitamin B12
iron deficiency anemia
Results when the intake of dietary iron is inadequate for Hbg synthesis
-most common in all age groups
-1 in 8 people worldwide
-common in vegetarians, gastrectomy, celiac disease, weight loss surgery
-developing countries (inadequate iron rich foods, intestinal parasites)
-united states (blood loss in perimenopausal women, men, and postmenopausal women)
-blood loss uses up iron stores (chronic alcohol use with GI tract blood loss)
symptoms of iron deficiency anemia
-smooth, sore tongue
-angular cheilitis
-brittle ridged nails
-low serum ferritin levels (iron stores are depleted)
-MCV decreased (decreased iron stores cause production of small RBC)
-Hgb, Hct, and RBC low
Nursing diagnoses regarding iron deficiency anemia
-Fatigue r/t Hgb and diminished oxygen carrying capacity of the blood
-Imbalanced nutrition, less than body requirements, r/t inadequate intake of essential nutrients
-Activity intolerance related to inadequate hemoglobin and hematocrit
-Noncompliance with prescribed therapy
how to diagnose iron deficiency anemia
-Bone marrow aspiration is definitive, but rarely done (invasive and painful)
-Diagnosis can be made on summation of symptomatic history and iron studies
-Stool for occult blood
treatment of iron deficiency anemia
-oral iron supplement → take on empty stomach, don’t take with antacids/dairy/calcium, constipation or darken stools, vitamin C may increase absorption, iron stores take 6-12 months
-IV iron → small test dose to rule out anaphylaxis, epinephrine on hand
-IM iron → rare, use Z-track method to avoid skin stain
Anemia in ESRD
-Erythropoietin deficiency
-Blood loss thru dialysis machines
-Folate is dialyzed out
-treatment = Procrit or Epogen (iron supplements, try to maintain Hgb 11-12)
hemolytic anemia
erythrocytes have shortened lifespan
-hemoglobin broken down
-80% of heme is converted to unconjugated bilirubin
-lab results will show an elevated retic count, unconjugated bili is increased, leading to jaundice
-reticulocyte count elevated (immature RBCs)
inherited vs. acquired hemolytic anemia
inherited = sickle cells anemia, thalassemia, thalassemia major, G-6-PD deficiency
acquired = autoimmune hemolytic anemia, non immune-mediated hemolytic anemia, heart valve hemolysis, hypersplenism
secondary polycythemia
excessive production of erythropoietin
-may be caused by chronic hypoxia
-heavy smoking, COPD, OSA, high altitude, carbon monoxide exposure
secondary polycythemia s/sx and treatment
s/sx = rudder/redness, pain in hands and feet
treatment = reduce stimulus, therapeutic phlebotomy (500 mls once or twice a week)
causes of neutropenia
-Aplastic anemia from toxins or medications
-Metastatic cancers
-Myelodysplastic syndromes
-Chemotherapy
-Radiation therapy
-Risk for infection from exogenous and endogenous
-If pt is taking corticosteroids, that may not generate a fever with infection
neutropenia
neutrophil count less than 2000
-ANC (absolute neutrophil count)
-ANC less than 500 → high risk
-ANC less than 100 → greatest risk
treatment of neutropenia
depends on the cause
-Culture blood, urine, sputum, and XR
-Broad spectrum AB until the organism is identified
neutropenic precautions at the hospital
assess
report s/sx of infection
culture and sensitivity
private room with WBC less than 1000
no sick visitors
no rectal or vaginal procedures
stool softener
hygiene
food hygiene and safe food handling
change water pitcher, respiratory equipment containing water, denture cleaning fluids
neutropenic precautions at home
hand, oral, and body hygiene
skin integrity
avoid birdcages and litter boxes
consider avoiding gardening (soil) and fresh flowers in stagnant water
high calorie and protein diet, 3L fluid unless otherwise restricted
avoid crowds and sick people
Platelets
-Spleen holds about 1/3 of circulating platelets
-Primarily responsible for hemostasis from small vessels
-Lifespan of 8-11 days
-Low platelet count can lead to petechiae
thrombocytopenia
low platelet level
-reduced production (give platelets)
-increased destruction (treatment is splenectomy)
-increased consumption
-spontaneous bleeding/petechiae range 20-50
-risk for fatal hemorrhage less than 5
-risk of bleeding at higher count if platelets are dysfunctional from ASA or MDS
-# of platelets does not equate to clotting ability
primary thrombocytopenia
-Stem cell disorder within bone marrow
-Marked increased in platelets greater than 600,000 (may be dysfunctional)
-Affects women twice as much as men
-Median age of onset is 65-70
-May be asymptomatic until platelet count is greater than 1 million
-Hemorrhage (dysfunctional platelets) or vascular occlusion in deep veins and micro circulation
-Headaches*, TIAs, DVT, PE
quantitative platelet defects
thrombocytosis = elevated count
thrombocytopenia = decreased count
qualitative platelet defect
platelets are dysfunctional
medical management of platelet defects
eliminate precipitating cause, stop medication that is contributing, platelet transfusion
nursing management of platelet defects
OTC medication teaching, avoiding alcohol, notify healthcare providers
nursing interventions for thrombocytopenia
No ASA
No IM injections
No catheters
No rectal anything
Ambulate with the pt
Electric razors
Stool softeners
Smallest needle possible
No flossing
Lib lubricant
Gentle suctioning