Hematology Part 2

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  1. **Anemia
    • -"a deficiency in the number of erythrocytes, the quantity or quality of hemoglobin, and/or the volume of packed RBCs (hematocrit). --not a specific disease, more like a symptom of a underlying disorder
    • -leads to hypoxia because RBCs transport oxygen.
    • -Clinical Manifestations are caused by the body's response to hypoxia.
    • Deficiency in erythrocytes, quantity of hemoglobin, or volume of RBC’sNot a specific disease
    • S/S related to tissue hypoxia
    • Diagnosed by CBC, Reticulocyte count and peripheral blood smeaar (classified)
    • Classified by RBC indices: why type of anemia. Further workup to determine underlying cause

    • => Anemia Video:
    • RBCs made in bone marrow, has hemoglobin (red colored protein) which oxygen attach to. RBCs transport oxygen to cells and tissues. When empty, they attract Carbon Dioxide and other waste gases
    • Anemia occurs when little RBCs or not enough hemoglobin. Exhaustion & Fatigue is the common sign of Anemia!
  2. **Causes of Anemia
    • => Etiology  Three main causes of Anemia:
    • 1. Decreased erythrocyte production (not making enough RBCs)
    • -decreased or deficiency in Iron, Vitamin B12 or folic acid nutrients (malnutrition cause)
    • -Decreased erythropoiethin (hormone that's made in the kidneys)
    • -Decreased Iron availability in the liver. (Iiver isn't taking in as much iron)

    • 2. blood loss (acute and chronic)
    • - Chronic hemmorahage (GI tract, colon cancer)

    3. increased erythrocyte destruction ( aka hemolysis, (such as sickle cell); occurs with certain medication, blood transfusion reaction & Incompatible blood, or trauma to RBCs (going through Cardiac/Pulmonary Bypass Machine-Occurs during surgery) Or maybe through Dialysis (RBC destruction).
  3. => Clinical Manifestations Depends on degree of anemia: (THREE DEGREES)
    1. Mild anemia (Hbg 10 to 14g/dl): May be asymptomatic; may not know.

    • 2. Moderate anemia (Hbg 6 to 10g/dl):
    • Palpitations, dyspnea, diaphoresis (from body trying to compensate

    • 3. Severe (Hbg less than 6g/dl): Multisystem involvement; extremely serious, you can die.
    • -Clinical presentation depends onseverity, age, body's ability of heart's blood to compensate (decreased oxygen capacity of the blood)

    • -If hemoglobin is Less than 8, then you should be getting a blood transfusion!
    • -In older adults: mistaken from regular aging changes, overload of cormorbidities.
  4. **Severe Anemia: Signs/ Symptoms
    Pallor, jaundice, pruritus (itching of skin)

    • -Jaundice in Dark skin: Sclera and mucous membranes
    • Tachycardia, murmurs, angina, HF, MI, claudication( Spasming of the vessels)

    Tachypnea, orthopnea, dyspnea

    HA (head ache), vertigo, irritability, depression, parasthesias (numbness or tingling of lower extremities)

    Glossitis (smooth tongue), anorexia, hepatomegaly, splenomegaly

    Cold sensitivity, weight loss, fatigue

    • symptoms: Fatigue/weakness despite getting enough sleep. Stresss Situations. Pale skin (not enough oxygen skin in blood), being unfocused and scattered. And "Craving to chew" odd.n
    • -If it becomes serious: feels like HA: rapid breathing, irregular Heartbeat and chest pain o:
    • -Two easiest treatments: Iron supplements and Iron rich foods (liver, prune juice, clams, oysters, soy beans, tomato puree, lean meats)-Cook in iron skillets!
    • -accupuncture: wound stagnant blood
    • -sometimes overexercising can exacerbate anemia.
  5. **Anemia:  Diagnostics
  6. CBC
    • RBC indices
    • Peripheral Smear: take blood and smear it on the slides, and look at shape of RBC under microscope.
    • Iron studies
    • B 12 levels
    • Folate levels
    • Bone Marrow Biopsy
  7. **Anemia: Collaborative Care
    • Determine the causative factor
    • Correct and control the underlying disease
    • Patient education: important in diet and oral supplementation

    • => Acute interventions PRN:
    • Blood transfusions:
    • Drug therapy: IV Iron-blood therapies
    • Volume replacement
    • Oxygen therapy
  8. **Nursing Considerations: Blood Transfusions
    Verify physician order for blood product and informed consent; make sure they're aware of the s/s, risk/bnenefits, and when to call for assistance

    -when you first start a blood transfusion: stay with the patient for 15 minutes to monitor them for a reaction.

    Conduct thorough physical assessment and document

    Educate patient about blood transfusion

    Verify patent vascular access, assemble equipment

    • Start NS infusion at TKO, pre-medicate if ordered; two bags and the Y then pump then your patient.
    • -Spike the saline first, prime the Y line, then clamp so that you prime BOTH sides, back priming to the blood line.
    • - Prime all your lines and lines of patient with salline
    • -Then clamp saline bag
    • -Open blood bag so that blood can go through the pump and into the patient.
    • -So you're "lubricating" all lines with NS.

    Double-check blood product with SECOND RN in patient’s roomInfuse product per facility policy (MUST be infused within 4 hours)

    • -Once blood gets in the floor, it must be hung within 30 mins.
    • -need peripheral gauge of 20 or LARGER. 22 gauge is too small. Can cause hemolysis in the RBCs
    • -sometimes physicans will order premedication (benadryl and tylenol) to prevent any blood transfusion reactions, but helps with ultrasenstivity although they still might react..

    -Usual rate is 50 the kicked up to 100 cc's hr.
  9. **Types of Anemias
    • =>Anemia from decreased RBC production
    • Iron Deficiency Anemia
    • Thalassemia
    • Cobalamin (B12) Deficiency
    • Folic Acid Deficiency
    • Anemia From Chronic Disease
    • Aplastic anemia

    =>Anemia from acute blood loss

    =>Anemia from increased RBC destruction
  10. **Roles in Erythropoiesis:
    -Cobalamin (B12): RBC maturation

    -Coppr: mobilizsation of iron from tissues to plasma

    -Folic Acid: RBC maturation

    -Iron: Hemoglobin synthesis

    -Niacin: needed for maturation of RBC

    -Pantothenic Acid (B5)-Heme synthesis

    -Pyridoxine (B6): hemoglobin Synthesis

    -Riboflavin (B2): Oxidative reactions

    -Vitamin E: possible role in heme synthesis. Protection against oxidative damage to RBCs

    -AminoAcids: synthesis of nuceloprotiens

    --Ascorbic Acid (Vit C) - Conversion of folic acid to its active forms, aids in iron abosorption.
  11. **Iron Deficiency Anemia & Reasons it occurs
    • Most common chronic hematologic disorder
    • -1mg of iron lost daily through feces, sweat and urine.
    • --Certain groups are at increased risk: menopausal, pregnant women, low socioeconomic backgrounds, older adults, and individuals experiencesing bloodloss

    • =>Occurs secondary to
    • 1.Insufficient dietary intake

    2. Malabsorption: taking it orally but body isn't absorbing it.

    • 3. Blood loss 
    • Very young (menstruation), malnourished, and women of childbearing age are susceptible
    • -Bad dieting.
    • -GI is a frequent cause of iron deficiency because they're not abosorbing it, '
    • -Loss of 50-70 ml of blood from the upper GI tract is required for stools to appear black (melenta) which results from iron in the RBCs
    • -Peptic uler, gastritis, esophagitis, diverticuli, hemorrhoids and neoplasta: commmon causes of GI blood loss.
    • -GU blood loss occurss primarily from menstrual bleeding. THe avg monthly menstrual blood loss is about 45 mL and causes the loss of about 22 mg of Iron.
    • -Dialysis treatment may INDUCE iron deficiency anemia because of the blood lost in the dialysis equipment and frequent blood sampling.
    • -2 Mls of blood usually contain 1 mg of iron. Menstruating women loss 22 mg of iron a month D:
    • -WE try to give Iron supplements with Vitamin C! with OJ!! c:

    4. Hemolysis
  12. **Iron Deficiency Anemia: Clinical Manifestations
    • May be asymptomatic initially
    • General manifestations of anemia
    • Pallor is the most common finding
    • Glossitis is the second most common (smooth, red tongue)- caused by atrophy of the papillae or destruction of tongue taste buds

    Chelilitis-Inflammation of the lips Concave (spoon-shaped) fingernails: impaired metabolary circulation

    Pica: ingestion of nonfood substances.
  13. **Drug Therapy: Iron Oral & IM.
    1. Iron absorbed best from the duodenum and proximal jejunus: so enteric coated/SR which release iron farther down in the GI tract are counterproductive

    2. Daily dose should provide 150-200 mg of elemental iron.

    3. Best absorbed as ferrous sulfate in an acidic environment. For this reason, an to avid binding the iron with food, iron should be taken about an ohours before meals, when the duodenal mucosa is most acidic. Taking iron with vitamin C or OJ, enhances iron absorption.

    4. Undiluted liquid iron can stain teeth--should be diluted and sipped with straw

    5. GI side effects: Heartburn, constipatio and diarrhea.

    • => IM: given for malabsorption, intolerance of oral iron, or poor patient adherence
    • -Sodium ferrous gluconate and iron sucrose are altenratives--carry less risk of life threatening anaphylaxis.
    • -IM iron can stain skin: separate needdles should be used for withdrawing the solution and for injecting the medication. Use Z-track injection.
  14. **Iron Deficiency Anemia: Diagnostic studies (how does it show in CBC and Indices)
    =>CBC: Decreased RBC, Hgb, Hct

    • =>RBC indices
    • Decreased MCV, MCH, MCHC
    • Increased RDW-RBCs will be wider in diameter

    • =>Iron studies
    • Low serum iron and ferritin
    • Elevated TIBC (total iron binding capacity)
    • -Decreased transferrin: protein that hooks up with the iron.

    • Other Diagnostics
    • Bone marrow aspiration/biopsy: Most definitive in diagnosing “production classification” of anemias
    • Stool guaiac test: occult blood in stool (get stool piece on card, put solution on it, so if it turns blue= IRON/BLOOD somewhere in stool where it shouldn't be)
    • Endoscopy: down esophagus and stomach, duodenlum for ulcers
    • Colonoscopy: look for tumors, polyps in the colon.
  15. **Collaborative Care: Iron Replacement = GOAL.
    • =>Dietary
    • Red meat, fish, green leafy vegetables, beans, dried fruits, molasses, fortified carbohydrates
    • Vitamin C enhances absorption

    • =>Oral
    • Ferrous sulfate 325 mg PO TID
    • Best given in acidic environment (SO BEFORE Meals-take on EMPTY stomach!) but can cause nausea
    • SE: can turn stoool black (black stool usually means blood in stool)
    • -Drug interactions: don't take it with antacids, dairy products, and caffeine--all decrease effectiveness of Iron. So wait an hour before administration times.

    • =>Parenteral
    • Iron dextran, gluconate, sucrose IM or IV- Intermitten IV, small primary bag hung for hour with temp tubing (brownish/orangish)
    • -Iron itself isn't compatible with anything btw
    • Risk for anaphylaxis: sometimes test doses are order
    • -SE: headache, BP changes, usually continue Iron therapy orally after hemoglobin has normalized.
  16. **Thalassemia
    Autosomal recessive genetic disorder; common in mediterranean descent, regions of asian and aftrica-autosomal recessive means: you need copies from both parents!

    • =>Results in insufficient Hgb production due to absent/decreased globulin chains (TWO TYPES)
    • Heterozygous- thalassemia minor/trait (one copy of gene is mutated)
    • Homozygous- thalassemia major (BOTH COPIES of genes are mutated.

    • Found in ethnic groups by the Mediterranean Sea, regions of Asia/Africa
    • -all newborns screened for this in birth
  17. **Thalassemia TYPES: Major vs Minor
    • =>Thalassemia major (homozygous- gene from BOTH parents)
    • Life threatening!
    • Significant physical and mental growth retardation
    • S/S of severe anemia
    • Hepatosplenomegaly: INCREASED liver and spleen size
    • -hemolysis of RBCs causes enlargement of liver, spleen and jaundice
    • Jaundice: body is trying to compensate for disease process from the hemolysis of RBCs
    • Chronic bone marrow hyperplasia
    • -As bone marrow respons to the reducesd O2 carrying capacit y of blood, RBC production stimulated and the marrow becomses bpacked with immature erythroid precursors taht die.
    • -> Stimulates further erythropoiesis --> leading to chronic bone marrow hyperplasia and expasion of the mrrow space; this may cause thickening of the cranium andmaxillary cvity.
    • -Thrombocytosis after spleen dysfunction and/or removal may occur

    -Thalassemia patients may have Hepatitis C: due to blood transfusions received before hep C sccreening in 1992.

    =>Thalassemia minor (heterozygous- gene from ONE parent)

    • Often asymptomatic with mild to moderate anemia with microcytosis (small cells) and hypochromia (pale cells)Mild to moderate microcytic, hypochromic anemia
    • -CBC count shows mild to moderate
    • -no treatment b/c the body adapts to the reduction of normal hemoglobin
  18. **Thalassemia: Collaborative Care
    • Diagnosed via CBC and Hgb analysis
    • No specific drug or diet is effective in treating thalassemia

    • =>Thalassemia major
    • Collaborative care: Blood transfusions and exchange transfusions
    • Given with chelating agents PO, IV (because blood transfusions causes overload of IRON aka hemochromatosis so chelation helps keep iron at normal level)
    • -GOAL: is to keep Hgb at 10g/dl so there's no iron overload (to maintain the patient's own erythropoiesis without causing the spleen to enlarge; zinc supplementation may be needed sincezinc is reduced with chelation therapy)
    • Supplements PRN: folic acid, zinc and vitamin C to help rebuiild RBCs, NO Iron Suupplements!
    • Splenectomy PRN: Because RBCs are sequestered in the enlarged spleen.
    • -ONLY ONE CURE: hemopoietic stem cell transplatation: but it's hard to find a match and lots of risk with that procedure ):
    • -patho: they're not making hemoglobin like they should, it's an abnormal hemoglobin that doesn't carry oxygen due to ddecreased affinity.
  19. **Megaloblastic Anemia
    Group of disorders caused by impaired DNA synthesis; Characterized by the presence of large RBCs (megaloblasts)

    -when DNA synthesis is impaired, defective RBC maturation results.

    -RBCs are large (macrocytic) and abornal and are reffered to as megaloblasts.

    -Macrocytic RBCs are easily destoryed because they have fragile cell membranes. Although the overwhelming majority of mealoblastic anemias result from cobalamin and folic acid defifiencys, this type of RBC deformity can also occur by drugs, inborn errors of cobalamin and folic acid metabolsim and erythroleukemia (malignant blood disorder characterized by a proliferation oferythropoietic cells in bone marrow.

    • =>Majority result from deficiency in
    • Cobalamin (vitamin B12)
    • Folic acid
    • -Occurs from suppression of DNA synthesis by drugs or inborn errors of cobalamin and blood cell metabolism
  20. **Cobalamin (Vitamin B12) Deficiency:
    • -Normally, A protiein termed intrinsic fafvtor (IF) is secreted by parietal cells of the gastric mucosa. IF is required fro cobalamin (extrinsic factor) absorption.
    • -CObalamin is normally abosrbed in the distal illuem
    • -THEREFORE if IF is not secreted, cobalamin witll not be absorbed.

    • => CAUSES:
    • 1. Most common: Pernicious Anemia.
    • 2. GI surgery (gastrectomy, gastric bypass)
    • 3. Bowel resections involving the illeum
    • 4. Chron's disease, ileitis, celiac disease, diverticuli of the small intestsic or chronic atrophic gastritis. (Cobalamin deficiency results from the loss of IF secretion gastric mucosal cells or impaired abosrption of cobalamin in the distal ileum)
    • 5. Found in chronic alcoholics, long term uses of H2-Histamine receptor blocks and proton pump inhibitors
    • 6. Strict vegetarians.
  21. **Pernicious Anemia:
    THe most common cause of cobalamin deficiency; caused by an absence of IF. THe gastric mucosa is NOT secretic IF because of either gastric mucosal atrophy or autommine destruction of pariental cells.

    -parietal cells secrete HCL also, in pernicious anemia, there is decrease in HCL. (NOTE: Acid environment in the stsomach is required for secretion of IF)

    -Pernicious anemia is a disease of insidious onset that begins in middle age or later (after age 40, 60 years being most frequent)
  22. **Cobalamin (B12) Deficiency: Occurs secondary to:
    =>Decreased intake; easily fixed by fixing intake as long as you have intrinsic factor

    • =>Deficiency in intrinsic factor; more dangerous
    • -intrinsic factor ( a protein) is made by stomach and needed to absorb vitamin B12 in distal illeum)
    • -Ulcer causes deficiency in intrinsic factors
    • -Can lead to Pernicious anemia: "Highly destructive"
    • -autoimmune disorder can cause loss of intrinsic factor
    • -Most people 60 years old when diagnosised
    • Gastrectomy: decreased intrinsic facotr b/c no stomach lining
    • Chronic gastritis
    • Chronic PPI/H2 blocker therapy: Causes lack of instrinsic factor.

    • =>Intestinal malabsorption
    • -Presennce of gastric factor is needed to break down and absorb B12, chronic H2 blockers or PPI, don't have ability to absorb B12.
  23. **Cobalamin Deficiency:Clinical Manifestations
    General s/s of anemia; related to cobalamin deficiency develop because of tissue hypoxia.

    GI: glossitis, anorexia, N/V, abdominal pain

    Neuro: weakness, paresthesia, numbness, ataxia, impaired thought processes

    • -prounounced the most with pernicous anemia
    • -lack of vitamin B12
  24. **Cobalamin Deficiency: Diagnostic Studies

    Peripheral smear/RBC indices: Macrocytic anemia

    Serum B12 and folate levels usually decreased

    Serum test for anti-IF antibodies- : specific for pernicous anemia

    Methylmalonic acid and homocysteine levels-deficiencies cause more risk for pernicious anemias.

    Schilling test: NOT really used with anemia, basically differentialtes if people have anemia or just absorption problem

    --Serum folate level: If they are normal and cobalamin levels are low, it suggests that megaaloblastic anemia is due to acobalamin dieficiency.

    -Uppier GI endoscopy and biopsy of the gatric mucosa may also be done due to potential gor gastric cancer increased in pernivous anemia.
  25. **Collaborative Care: B12 replacement
    • =>Oral replacement usually not adequate ( pt is not able to absorb obalamin if IF is lack or if absorption in the illeum is impaired)
    • Well-balanced diet should be emphasized
    • Animal products high in B12
    • B12 supplement, fortified products for vegans

    • =>Intramuscular or intranasal cobalamin therapy (especailly for lack of intrinsic factors)
    • Daily x 2 weeks; Weekly until Hct normal
    • Then lifetime monthly treatments
    • -bypass GI tract, giving it straighn
    • -IM B12: bright red color.
    • -nasal spray: contraindicated if someone has allergies.
  26. **Folic Acid Deficiency Anemia (Megoblastic Anemia Cause) & Manifestations
    => Folic Acid: required for DNA synthesis leading to RBC formation and maturation

    -clincial manifestations similar to cobalamin deificiency: insidious, GI disturbances: dyspepsia, and smooth, red tongue.

    -Diagnostic findings: Serum folate level is low and serum cobalamin level is normal

    -Folic acid deficiency is streated by replacement therapy, the usual dosage is 1 mg/day by mouth.

    -the absences of neuro problems is an important diagnostic finding, it differentiates folic acid deficiency from cobalamin deficicnecy!!

    Almost always caused by inadequate intake: Leafy green vegetables, beans, grains, liver

    • Increased demand secondary to pregnancy, growth spurts, malignancy, chronic inflammatory disorders
    • -body can only store a small amount relative to daily requirements so you basically need it everyday.

    Decreased absorption with malabsorption syndromes, drugs such as methotrexate

    • Loss during hemodialysis
    • -elderly and alcoholics are most susceptible to this type of anemia
    • -alcoholism interferes with absorption AND increases excretion (storage problems)
    • -nutrient bag

    • **Folic Acid Deficiency: Clinical Manifestations
    • Insidious onsetGI s/s similar to cobalamin deficiencyNo neurological problems
  27. **Folic Acid Deficiency Anemia: Diagnosis & Collab Care
    • => Diagnosis
    • CBC, RBC indices
    • Macrocytic anemia
    • Serum folate and B12 levels

    • =>Collaborative care
    • 1-2 mg folic acid PO QD 4-5 weeks
    • Maintenance therapy with 1mg PO QD if needed
    • Dietary counseling: increase Folic acid intake
    • Alcoholism counseling!
  28. **Megaloblastic Anemia Nursing management:
    -pernicious anemia should be evaluated if there's a family hisotry

    -no prevention but early detection and treatment can lead to reversal of symptoms.

    -diminished sensitivity to head and pain resulting from neuro impairment: protect pt from falling , burns, trauma.

    -Gastric cancer screenings for pts wtih atrophic gastriitis related pernicous anemia.
  29. **Anemia of Chronic Disease
    -aka anemia of inflammation; general term for anemias that can be due to lot of disorders

    ex: renal disorder leads to decreased erytrhopoietin causing this anemia of chronic diseas as ex.

    Normocytic (normal size), normochromic, hypoproliferative anemia

    -Diagnosed by exclusions

    -Differentiated from other anemias b/c: elevated serum ferritin and increased iron stores (distinguish from iron deficiency anemia) and normal folate and cobalamin blood levels (distinguish it from megaloblastic anemia)

    Associated with inflammatory, autoimmune, infectious, endocrine and malignant disease

    Usually immune drivenDiagnosis of exclusion

    Treatment focuses on underlying disorder--if anemia is severe, blood transfusions may be indication; SHORT TERM but not for long term treatment.

    -Erythropoietin therapy (epogen) is used for anemia related to renal disease and may be used for anemia related to cancer, use conservatilively b/c of increased risk of thromboembolism and death.

    Associated with underproduction of RBC’s, and shortened RBC lifespan
  30. **Aplastic Anemia
    • -normocytic, normochromic (amt of hemoglobin)--the cells look okay, there's just not ENOUGH of them!
    • -term for pancytopenia due to bone marrow failure ; result from supression of bone marrow-disease in which the pt has eripheral blood pancytopenia (decrease of ALL blood cell tyypes: RBCS, WBCs and platelets) and hypocellular bone marrow.

    -ranges from chronic to critcal

    -chronic: managed with erythropoietin or blood tranfussions

    -Critical conditon: hemorrhage and sepsis. Pancytopenia d/t bone marrow failure

    • Congenital-birth vs acquired (70%--idiopathic) occurs from chemical exposure, occupational chemo/radiation and certain infections.
    • Can occur abruptly or insidiously,
    • Clinical manifestations range from mild to severe

    -diagonosed with low reticulocytes (immature RBCs); bone marrow biopsy to diagnose failure of production (from hip, should be red bone marrow but may see an increase in yellow bone marrow. Normal bone marrow has 30-70% blood stem cells, but in Aplastic--these cells are mostly gone and they've been replaced with fat.)

    • => Etiology: congential or acquired
    • -Acquired: idiotpathic or immune, chemical toxins, drugs (antiseizures, antimicrobials), Radial, VIral/bacterial infections like hepatitis

    • => Clinical manifestations:
    • -can be abrupt (days) or insidiously over weeks-months, range from mild to severe
    • -symtpoms caused by suppression of any bone marrow elements
    • -Fatigue and dyspnea, cardiovascular, and cerebral responses

    • =>Diagnostics
    • CBC/RBC indices
    • Bone Marrow biopsy
    • -hemoblobin, platelet values decreased
    • -RBC indices generally normal
    • -Normocytic, normochromic anemia.
    • -Low reticulocyte count and PRLONGED BLEEDING.
    • -Iron studies: TIBC and serium iron may be elevated as inital signs of erythropoiesis supression.
  31. **Aplastic Anemia Collaborative Care
    Remove the causative agent once you determine one they do, mild cases don't really need any treatment

    Supportive care until pancytopenia reverses (blood transfusions, oxygen, support body in it's own healing)

    -Decreased WBCs: protect them from infection, might be on neutropenic precautions

    • => Severe anemia
    • -Treatment: Immunosuppressive therapy (ATG, Cytoxan)--If the body is attacking the cells of the bone marrow, then prescribe AntiThyrociteGlobulin or Cytoxan.

    -Cure: Stem cell replacement; HSCT with a HLA-matched donor-Difficult to find a match (replacing all cells in body with donor cells)

    Ongoing blood transfusions
  32. **Anemia from Acute Blood Loss
    -normochromic, normocytic anemia--cells are fine, just being lost

    -If the acute loss is more gradual, the body maintains its blood volume by slowly increasing the plasma volume. Although circulating fluid volume is preserved, the number of RBCS available to carry oxygen is significantly diminished.

    -Trauma patients!! Sudden hemorrhage from trauma, surgery, vascular disruptions

    -Immediately in ER: Running warm saline by gravity, large bore IV--18 to 16 to replace the fluids. Later on get O- blood.

    -major concern: HYPOVOLEMIC SHOCK (Prevent by giving them fluids)s/s depend on % of volume lost; initially saline will dilute the hematocrit (Sometimes lactated ringers-for electrolytes)

    -Internal hermmorrhage may cause pain b/c of tissue distension, organ displacement and nerve compression, pain may be localized or referred.

    • =>Goals of collaborative care
    • Replace blood volume
    • Identify source/stop hemorrhage
    • Correct anemia: Blood transfusions (packed RBCS), supplemental iron may be required. No long term treatment necessary

    note: once volume replacement is established, attention can be directeed to correcting the RBC loss. takes body 2-4 days to manufacture new RBCS
  33. **Chronic Blood loss:
    -Similiar sources to iron deficiency anemia (bleeding ulcer, hemorrhoids, menstrual and PMS blood loss)

    -SE r/t depletion of iron sotres and considered iron-deficiency anmia.
  34. **Sickle Cell Disease
    -group of inherited autosomal recessive disorders characterized by an abnormal form of hemoglobin in the RBC-usually identified in childhood

    -Hemoglobin S causes the erythrocyte to stiffen and elongate, taking on a sickle shape

    -Sickle Cell traint occurs when a person is heterozygous for emoglobin S, the person has inherited hemogloin S from one parent and normal hgb A from other parent.

    -Sickling episodes: triggered by low oxygen tension in blood. Hypoxia or deoxygenation of RCs can be caused y viral or bacterial infection, high altitiude, emotional or physical stress, surgery and blood loss-Infection is most common cause of hypoxia

    -Dyhydration, increased hydrogen ion (acidosis), increased plasma osmalility, decreased plasma volume, and low body temp can cause or sustain sicklling episodes

    • -Sickling causes occlusion--> acute or chronic tissue injusy and results in hemostasis (self perpetuating cycle of local hypoxia and more sickle)-sickle cells hemolyzed by spleen.
    • -Vasoocclusive phenomena and hyemolysis are the clinical hallmarks of SCD

    => Vasoocclusive Crisis: Sickled cells impairs blood flow causing vasospasm, further restricting blood flow. Severe capillary hypxoia causes changes in membrane permeability, leading to plasma loss, hemoconcentration, thrombi and further circulatory stagnation. Tissue ischemia, infarctionand necrosis eventually occur from Oxygen lack.

    -SHOCK is possicble, life threatening consequenc of sickle cell crisis

    => Manifestations: Pain is primary. Anemic but asymptomatic exccept during sickling episodes. Jaundice is common (from hemolysis) and pats prone to gallstones (cholelithiasis)

    • =>Infection is a MAJOR commplication, cause of morbidity and mortality in patients.
    • -Spleen fialure to phagocytize foreign substance as it becomes infracted and dysfunctiional), spleen becomes SMALL due to repeated scarring (autosplenctomy)
    • -Pneumonia is most common infection; can cause aplasstic and hemolytic crissis and gallstones
    • -Acute Chest sydnrom: describes acute pulmonary complication, tissue fnfarction and fat embolism
    • -Pulmonary infarction: cause pulm htn, MI, HF, COR PULMONALE.
    • -Heart may become ischemia and enlarged--> HF-Injured kidenys from increased Blood viscosisty and lack of Oxygen.
    • -Priapism: persistent erection due to vein occllusion in penis.

    • => Collaborative Care:
    • 1. Alleviate symtoms
    • 2. Minmize end-organ damage
    • 3. Teach: avoid high altitudes, dddrink fluids, teat infections, immunizations

    • => Treatments:
    • -Hydroxyurea: chemo drug;; increases production of fetal hemoglboin, decreases reactive nutrophil count and increases RBBC volume.
    • -Hematopoietic stem cell transplation is the ONLY aviaialbe treatment that cute some pts
  35. **Hemolytic Anemia & Clinical Manifestations
    Destruction or hemolysis of RBCs at a rate that exceeds production (Ex: Sickle Cell)

    Can be classified as intravascular or extravascular

    Spleen is the primary site of destruction of RBCs that are old, defective or moderately damaged.

    Intravascular: RBC defects, usually hereditary (ex sickle cell disease-where cells are actually damaged and they sickle)

    Extravascular: Acquired, RBCs damaged by external factors (caused by maybe damage to spleen, prosthetic machines-dialysis machine or cardiopulmonary machine. Medications can damage. Macrophages are being destroyed as well.

    • =>Clinical Manifestations
    • Jaundice: Destroyed RBCs cause increased
    • bilirubin-yellow skin and eyes (breakdown of Hgb)
    • Hepatosplenomegaly: Liver and Spleen enlarged, Due to hyperactive with macrophage phagocytosis of the defective RBCs (increased size, congested with cells)
    • Acute Tubular Necrosis: Kidney damaged due to accumulation of hemoglobin molecules can obstruct renal tubules; cause decreased perfusion of kidneys and tissue necrosis
    • -main goal: keep kidneys functioning
  36. **Hemophilia
    • =>X-linked recessive genetic disorders caused by defective or deficient coagulation factors (more common in men)
    • -result in spontaneous mutations.
    • Hemophilia A: factor VIII deficiency (80%)
    • Hemophilia B: Christmas disease, factor IX deficiency (10-15%)
    • von Willebrand disease is a related disease-lack of coagulation protein that forms a complex with factor 8.

    • =>Life expectancy increased dramatically last century; mostly occured in children who never lived long enough to pass on their genes but now the life expectancy is longer.
    • -in past, they died from contaminated blood transfusions & HIV. But that stopped in 1987.
    • -Girls are carriers, and boys have 50% chance of getting it due to x/y
    • -interntal bleeding is more serious--into joints and tissues, swelling, painful,
    • -treatment: replacing missing factors (through donated plasma or genetically engineered recombinant).
    • -mild hemophilliacs aren't usually diagnosed until they're adults.
  37. **Hemophilia: Clinical Manifestations & Diagnostics
    Prolonged bleeding from minor trauma and injuries; irritations from brushing their teeth to hard

    • => Manifestations:
    • Uncontrollable hemorrhage after dental extractions
    • Excessive menstruation
    • Epistaxis-nose bleeds
    • GI bleeding from ulcers and gastritis
    • Hematuria & potential renal failure
    • Ecchymosis and subcutaneous hematomas-minor bumps and bruises
    • Hemarthrosis-bleeding in joints--> jt injury and eformity severe to cause crippling
    • Cranial bleeds

    • **Hemophilia Diagnostic Studies
    • Clotting factor tests (factor assays): required for definitive diagnosis of which factor is missing.

    Bleeding time

    PTT prolonged-reflects intrinsic factor

    PT/INR is normal

    CBC: Normal unless bleeding causes anemia (unless they're having an active bleed)
  38. **Hemophilia Collaborative Care
    =>Apply direct pressure/ice to stop bleeding

    =>Administer specific clotting factor: Also given as prophylactic measures

    • =>Rest affected joints until bleeding ceases, then they neeed to do ROM's so motion will increase healing time
    • NWB until swelling resolved
    • Resume ROM after bleeding stops to prevent deformity

    =>Analgesics PRN

    • =>Desmopressin acetate (DDAVP): usually given for mild hemo or VonWillebrand.For mild Hemophilia A/vWB disease
    • IV, SQ, intranasal spray
    • -Basically DDAVP acts on endothelial cells to release tissue stores of factor 8  :)
    • The effects only last only 12 hours, given in an acute setting after injury

    => Antifibrinolytic therapy: inhibits fibrinolysis by inhibitting plasminogen activation in the fibrin clot, thereby enhancing clot stablilityy

    =>Genetic counseling

    • =>Patient precautions
    • Wear med alert ID (bracelet/necklace)
    • Carry med alert ID in wallet/purse/glove compartment in car
    • Noncontact sports
    • Appropriate protective gear
    • Avoid NSAIDs, alcohol, certain herbs
  39. **Anemia: Nursing Diagnoses
    Activity intoleranceFatigueImbalanced nutrition: less than body requirementsDeficient fluid volume Ineffective therapeutic regimen managementIneffective tissue perfusionRisk for injuryPain
  40. **Anemia: Nursing Goals
    Assume normal activities of daily living: Measurable statement:

    Maintain adequate nutrition: Measurable statement; Pt. will demonstrate compliance with POC

    Develop no complications related to anemia (hypoxia)
  41. **Anemia: Nursing Interventions
    Dietary and lifestyle changes

    Blood or blood product transfusions

    Drug therapy: B12 injections or tablets, vitamins, folic acid, iron

    -Parasthesias in Cobalamin Deficiiencies.

    Oxygen therapy

    • =>Patient teaching
    • Nutrition intake: foods high in B12.
    • Compliance with drug therapy: oxygen
    • Limit alcohol intake: decreases body's ability to make RBCs and folic acid production
  42. **Thrombocytopenia:
    reduction of platelets below 150 K, result in abonrmal hemostais manifests as prolonged bbleeding aor spontaneous bleeding

    -Commonly acquired

    • => Immune throocytopenic Purpura:
    • primary autommine disorder--macrophages destroy platelets (corticosteroids suppress immune)

    • => Heparin Induced Thrombocytopnia:
    • typeically developed 5-10 days after hep therapy; major clinical problem: venous thrombosis and pulmonary embolis
    • -platelet aggregation also induces heparin to be neutralized, thus more heparin is required to maintain therapeutic activated partial thrombolastin times (aPTT)
    • -Clinical manifestatisons: epistaxis, mucosal bleeding, petechia, prlonged bleeding after injections, hemmorrhage (major chomplication--plt transfusions)
    • -Lab values: megakaryocytes (percusors to platelets) will be normal or increased)
    • -"Direct thrombin inhibitors", plasmapheresis to celar the plt aggregating igG from blood, protamine sulfate to interrupt circulating heparin
  43. **Neutropenia:
    -Leukopenia: decrease in total WBCS (grnulocytes, nonocytes and lympocytes)

    -Granulocytopenia: deficiency of granulocytes include neutrophils, eosonosphils and basophils

    -Neutrphils: majaor roles in phagocytizing pahtogenic microsbes--indicatior of pts risk for infection

    -ANC: determined by multiplyin the total WBC count by the percentage of neutrophils.

    • -Neutropenia: ANC less than 1 K! (normally: 2200-7700) and SEVERE: <500.
    • -Know if it's gradual or rapid: the faster the drop ad the longer the duration, the greater likelihood of life-threatening infection, sepsis or death
    • -Most common causes of neutropenia: chemotherapy and immunosuppressive therapies in the treatment of malignancyies and autoimmune diseases

    -"Nadir"- the lowerst point of neutropneia and other olood cells in a pttreated with chemo.

    • => Clinical meanifestations
    • -Infections can occur with oppurtunistic and nonpathogenic organisms from normal body flora
    • -WBC count depressed so nomral phagocytic mechanisms are imapired
    • -Classic signs of inflammation may not occur, NO PUS (no xray pulm infiltration)
    • -when there's a fever: assume caused by infection and requires immediate attention--> minor infections can lead to sepsis.
    • -consider any minor complaints of pain -> sepsis in MINUTES.
    • -Pneumonia: aspiration risks from normal flora /:

    • =>Diagnostics:
    • -Leukopenia: WBC <4K-Need the differential for <1K in neutrophils
    • -Peripheral blood smear to assess for immature WBCs (bands)

    • 1. Determine Neutropenic cause
    • 2. Identify offending infection organsim
    • 3. Institute antibiotics (can be prophyllactic)
    • -Aminooglycoside SE: oto and nephroxtoxicity
    • -Cephalosporins: rashes, fever and pruitius
    • 4. Administer hemapoietic growth factors (G-CSF granulocyte colony stimulator factor-, Neulasta, Neupogen)
    • 5. STRICT Handwashiing, single pt room, positive pressure or high efficiency particulate air (HEPA) filtration, community isolation if outpatient, Avoid uncooked meat
  44. **Leukemia:
    general term used to describe a group of malignant disorders affecting the blood and blood forming tissues of the BONE MARROW, lymph system, and spleet
  45. **Lymphomas:
    Malignant neoplams originaating in the bone marrow and lymphatic structus resultin in the polieraation of lymphocytes.
Card Set:
Hematology Part 2
2015-04-23 03:34:53
NS2 NSP2 Hematology Blood Anemia

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