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NSG 6665 Test 2: Hematology Questions With
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hematologic system - ANSWER massive fluid organ that permeates the entire body normal H&H newborn - ANSWER 14- 45-65%when do infants H&H drop - ANSWER 2-4 mo physiologic anemia - ANSWER normal drop in H&H of newborn normal hemoglobin makeup - ANSWER 2 alpha chains and 2 beta chainsnormal H&H 3 mo - ANSWER 9.5-14.5 and 31-41% normal H&H 6 mo-6yo - ANSWER 10.5-14 and 33-42%normal H&H 7-12 yo - ANSWER 11-16 and 34-40% retic from 3 mo on - ANSWER 1% decrease in hemoglobin may cause - ANSWER decrease in RBC productionWBC compared to RBC - ANSWER white larger and less of them newborns WBC vs adults - ANSWER newborns have more WBC and gets less as you getolder until 12yo what kind of infants need more H&H screens - ANSWER premature and low birth weight H&H risk factor screening questions - ANSWER low scoioeconomic status, low birthweight(<1500 g), cows milk before 6 mo, low iron formula, low intake of iron foods when to do H&H screens - ANSWER -if no risk factors, 9-12 mo, 6 mo later, and annuallyages 2-5 yo -LBW: before 6 moanemia - ANSWER a deficiency of red blood cells anisocytosis - ANSWER presence of red blood cells of unequal size poikilocytosis - ANSWER condition characterized by red blood cells in a variety ofshapes childhood and adolescence anemia types - ANSWER macrocytic, normocytic, and
hemolytic Microcytic anemia - ANSWER defect in hgb or globin synthesis Thalassemia - ANSWER Defect in a globin production (one of 4)genetic disorder Types of microcytic anemia - ANSWER Iron deficiency (late) ThalassemiaLead poisoning (plumbism) iron deficiency anemia - ANSWER A hypochromic, microcytic anemia characterized bylowered hemoglobin content of red blood cells and decreased numbers of red blood cells. most common hematologic disease of infancy and childhood - ANSWER iron deficiencyanemia most common anemia - ANSWER iron deficiency anemia most cost-effective test for iron deficiency anemia is - ANSWER CBC age of CBC for anemia check - ANSWER 12 moiron deficiency anemia etiology - ANSWER vInsufficient available iron for hemoglobin synthesis because of inadequate iron stores at birth due to prematurity, maternal orfetal bleeding, or maternal iron deficiency vInsufficient dietary iron to meet requirements of expanding blood volume duringperiods of rapid growth •Iron loss: occult, hemorrhage GI blood loss causes - ANSWER IDA NSAIDS and iron - ANSWER NSAIDS also deplete iron stores and contribute to irondeficiency anemia iron stores at birth adequate until - ANSWER 3-6 months How much ferrous sulfate per day - ANSWER 3-6mg/kg/day of elemental ironwhen to limit formula - ANSWER iron deficiency - limit to <24 oz per day to encourage solid food biggest risk for IDA age group - ANSWER <24 mo, especially 9-18 moiron deficiency and lead poisoning affect what - ANSWER brain development - brain 95% of adult size by 2 yo
continue for 2 to 3 months to normalize the Hgb and another 2 to 4 months to replacedepleted stored iron
Education on iron supplements - ANSWER •Give between meals for better absorption •Use straw or dropper to place liquid in back of mouth to reduce teeth staining in infants and small children •Given with juice containing Vitamin C increases absorption •Rinse mouth after taking when to switch from liquid to chewable vitamins - ANSWER by 36 mo iron in breast fed infants - ANSWER Exclusively breastfed term infants should receive 1mg/kg/day of elemental iron (15 mg max) beginning at 4 months and continue until iron containing foods are introduced iron deficiency and led - causes an increased absorption of lead ANSWER •Iron deficiency anemia is common in children and Lead molecules block iron from binding, inhibits essential membrane function, andinterferes with enzymes.
lead and pregnancy - ANSWER •Lead crosses the placenta •pregnant women who are exposed to lead may pass it on to their unborn fetuses. •Fetal absorption may be the cause of up to 50% of the lead ingested by the child.
- toxins during this time may affect the continuing development of the child after birthThe prenatal period is crucial to the development of the fetus, and exposure to any
chelating medications and iron - ANSWER Chelating medications for lead toxicity willalso pull out iron, therefore iron supplements should be delayed until after these meds are completed. lead levels of harm and of s/s - ANSWER harm at 10 mcg/dl
s/s at >50 mcg/dl Lead poisoning symptoms - •Aggressive behavior ANSWER •Irritability •Low appetite and energy •Difficulty sleeping •Headaches •Loss of previous developmental skills (in young children) where is most lead stored - ANSWER most lead is stored in the bones and is notmeasured by the blood lead levels
lead poisoning level - ANSWER >10mcg/dl lead testing ages - ANSWER •At 6 months of age with + risk factor •Home built before 1960 •Parent(s) working in lead •Pica -related industry •Sibling or playmate with evidence of lead exposure •All children, including those at high risk, at 12 months of age •Medicaid insured - all children at 1 and 2 years of age (may vary by state) lead risk if home was built before - ANSWER 1960 lead paint or pipes lead poisoning reversible? - ANSWER no
macrocytic anemia - ANSWER due to folate or vitamin B12 deficiency or both macrocytic anemia types - ANSWER megablastic and hemolytic megablastic anemia - ANSWER folic acid or b12 deficiency or both hemolytic anemias - ANSWER sickle cell, spherocytosis, G6PD deficiency sources of folic acid - ANSWER Whole wheat, grains, beans, green vegetables, carrots,fruits, egg yolks, animal organs
risk factors for megaloblastic anemias - ANSWER Suspect megaloblastic anemia ininfants being fed powdered cow's milk products, goat milk, or children who are vegetarians, absorption problems, or tapeworm infestations. megaloblastic anemia age peak - ANSWER 4-7 m megaloblastic anemia s/s - ANSWER •Irritability, poor weight gain, chronic diarrhea •MCV markedly increased (>100 fL) •Retic decreased •Anisocytosis, poikilocytosis •Becomes clinically apparent within months Dx of megaloblastic anemia - ANSWER serum folate less than 3 (4-20 normal) folic acid dose - ANSWER 1-5 mg/day Megaloblastic Anemias: Folic Acid Deficiency follow-up -repeat CBC ANSWER •RTC 1 -2 weeks,
•Rapid reticulocytosis (peaks 5 -8 days) •Rise in Hgb and Hct in one week, should reach normal levels within 2 months folic acid prolonged use - ANSWER Prolonged use of high-doses of folic acid should beavoided. Patient may require a multivitamin with a maintenance dose of 0.2 mg of folate.
b12 dose - ANSWER 1 mg daily then 1 mg weekly x 4 weeks then 1 mg monthly Normocytic anemia - ANSWER •RBCs are normal size •RBCs are normal in color •Fewer in number Normocytic anemia exist with - ANSWER chronic illness, B 12 deficiency, traumaticblood loss, and pregnancy
one of the most common causes of anemia - ANSWER acute or chronic inflammation how long after infection does anemia resolve - ANSWER up to 4 weeks why does anemia of infancy occur - •Lifespan of fetal red cells ANSWER •Production of rbcs •Hemodilution from rapid growth labs of physiologic anemia of infancy - elevated ANSWER •MCV normal, retic normal or slightly •With minor infections Hgb may drop to 9 -10gm/dl physiologic anemia of infancy in premature infant - premature infants and is more severe ANSWER •Occurs earlier in
Hereditary spherocytosis presentation - ANSWER •Clinical presentation: variable •Neonate: significant jaundice and anemia •Smear will show spherocytic small RBCs •Most patients have chronic anemia (hgb 6 -10 gms/dl), mild jaundice and splenomegaly -Chronic fatigue, malaise, and abd pain may also be noted. Hereditary spherocytosis management - ANSWER •Treat febrile child •Refer for consideration for splenectomy (preferably >5 yrs of age) why are RBCs prematurely destroyed in the spleen with hereditary spherocytosis -ANSWER Hereditary spherocytosis is hemolytic anemia in which there is a deficiency or abnormality of RBC membrane protein spectrin. This causes the RBC's surface areas tobe smaller. These RBCs are prematurely destroyed in the spleen.
G6PD deficiency -decreases life span of RBCs which can lead to hemolysis following exposure to inciting ANSWER •Glucose -6-phosphate dehydrogenase deficiency agents G6PD deficiency significant if -exposure to drugs, infection occurs, or in the presence of DKA ANSWER • Deficiency may not be significant unless
G6PD deficiency transmission - ANSWER G6PD gene ifs found on the x chromosome andthe deficiency is transmitted as a X- linked recessive trait.
most common RBC metabolic disorder - ANSWER G6PD Deficiency clinical manifestations of G6PD Deficiency - ANSWER episodes of hemolytic anemia withvarying degrees of severity, jaundice, back pain, hemoglobinuria, dizziness, palpitations, and dyspnea -Patient usually has had a history of recent infection particularly hepatitis or oxidantdrug ingestion and degree of hemolysis is based on the amount of the drug ingested.
how soon after drug does G6PD deficiency occur - ANSWER 1-3 days to start ofsymptoms
Management of G6PD deficiency - hemolysis: ANSWER •Avoid food and drugs that cause •fava beans, aspirin, sulfonamides, high dose ascorbic acid, methylene blue, antimalarials, chloramphenicol, nalidixic acid, napthalene mothballs, primaquine •Transfusions normal platelet count in newborn vs adult - 150,000-450,000 mm3 ANSWER •Adult: •Newborn: 84,000-478,000 mm thrombocytosis - ANSWER an abnormal increase in the number of platelets in thecirculating blood
thrombocytosis risk factors - platelets ANSWER •Risk for hemorrhage caused by defects in •Increased risk for clotting •MI •CVA •Arterial occlusion anywhere •Thrombophlebitis Thrombocytopenia - ANSWER low platelet count Thrombocytopenia causes - ANSWER • Deficient platelet production
where does bleeding occur in hemophilia -occurs in muscles, soft tissues, joints and is delayed ANSWER • Bleeding in A and B typically •Bleeding in C is usually mucous membranes, or skin WBC by age - ANSWER Newborn: 9,000-30,000/ mm 3 months: 6,000-18,0006 mon-6yrs: 6,000-18, 7 - 12 years: 4,500-13,500Adult: 5,000- 10,000 / mm
the neutrophilic response - ANSWER leukocyte increase as a defensive mechanism inresponse to bacterial infections
Granulocytes - ANSWER neutrophils, eosinophils, basophils Agranulocytes - ANSWER lymphocytes and monocytes more granulocytes or agranulocytes - ANSWER 40-70% granulocytes major WBC in bacterial infection fight - ANSWER neutrophil s Eosinophils function - ANSWER -help moderate allergic reactions-defend against parasites
Basophils function - ANSWER viral infections Lymphocytosis - ANSWER abnormal increase in lymphocytes
Lymphocytosis cause - ANSWER viral infections neutropenia - ANSWER deficiency of neutrophils2 weeks-1 yo <
1 yo < neutropenia cause - ANSWER • reduced cellular production •increased peripheral destruction •severe bacterial infections
neutropenia manifestations - •malaise, fever, chills ANSWER •bacterial infections •weakness •agranulocytosis leukemia - ANSWER Malignant neoplasm of hematopoietic stem cells characterized bydiffuse replacement of bone marrow by neoplastic cells
blast cells - ANSWER leukemia baby cells neutropenia - ANSWER deficiency of neutrophils-extreme risk for bacterial infection -usually caused by chemo
most common childhood cancer - ANSWER leukemia - 26% of ped cancers <15 yo what do all leukemias have in common - ANSWER undifferentiated WBCs leukemia white count - ANSWER can be high, low, or even normal -test bone marrow
if one identical twin is dx with ALL how likely is the other - ANSWER 20-25% if dx before 6yo
what is the risk of a twin or sibling developing ALL - ANSWER 2-4x the risk when is an ALL pt considered cured - ANSWER after 10 years of remission AML - ANSWER acute myeloid leukemia aka acute non-lymphocytic leukemia (ANLL) average age of AML - ANSWER 15-39 yo 15% in children and 31% in adolescences AML tx - ANSWER bone marrow transplant common issues with AML and ALL - ANSWER •Anemia, thrombocytopenia, neutropenia leukemia s/s - •infections ANSWER •recurrent fever •pain in joints •lymphadenopathy •splenomegaly •fatigue •shortness of breath •pallor •easy bleeding or bruising and spots under the skin
•pain in the bones or joints
