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Chronic Alterations: Exam 1 > Module 2: Hematologic Conditions > Flashcards

Module 2: Hematologic Conditions Flashcards

1
Q

Normal Laboratory References

A

WBCs: 4.5-11

Platelets: 150-350

Hemoglobin: 13.9-16.3 (males); 12.0-15.0 (females)

Hematocrit: 41-53 (males); 36-46 (females)

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2
Q

Hematologic Disorders

A

Disorders of the hematopoietic system (production and maturation of RBCs, WBCs, and platelets)

Primary hematopoiesis:

  1. Hematopoietic cells are committed and developed in the bone marrow
  2. Primary disorders occur during cell development

Secondary hematopoiesis:

  1. Storage sites: Spleen and lymph
  2. Secondary disorders

Common hematologic disorders:

  1. Leukemia/lymphoma
  2. Anemia — Types: Blood loss, chronic illness, nutritional (iron, B12, or folic acid deficiencies), and sickle cell
  3. Thrombocytopenia
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3
Q

Assessment of Patients with Hematologic Disorders

A

Risk factors & PMHX:

  1. Genetic tendency
  2. Bone marrow depressing meds.
  3. Chemical or radiation exposure
  4. Infectious disease (especially viral)
  5. Nutrition

Suspicious S/S:

  1. Bleeding
  2. Bruising
  3. Pale/cyanotic
  4. Fatigue
  5. Fever
  6. Frequent infections

Physical examination is based upon risks and differential diagnosis

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4
Q

Diagnosis of Hematologic Disorders

A

Complete Blood Count (CBC):

  1. H&H, RBC count
  2. RBC indices (provide information about the Hgb content and size of RBCs) — differentiates nutritional anemias
  3. WBC count
  4. Platelets

Extended hematologic studies:

  1. Reticulocytes (immature RBCs)
  2. Iron studies — detect iron deficiency anemia
  3. Nutritional studies — i.e. folate level

Bone marrow biopsy (based on CBC) — it is performed if RBCs, WBCs, and platelets are all abnormal; extremely invasive (addresses leukemia)

Coagulation profile:

  1. Prothrombin time (PT)
  2. Partial thromboplastin time (PTT)
  3. Fibrinogen level

Chemistry tests (indicate hemolysis):

  1. LDH
  2. Bilirubin
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5
Q

Anemia

A

Inadequate RBC quantity or RBC dysfunction; classified by etiology and cell characteristics

CMs: Decreased oxygen-carrying capacity and tissue perfusion

Contributing factors:

  1. Hgb: Amount of heme protein that carries oxygen (best indicator)
  2. Hct: Measurement of how much of blood is made up of RBCs (affected by fluid volume)
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6
Q

Reticulocytes

A

Relatively immature precursor to mature RBC

Indicative of:

  1. RBC turnover (bone marrow release of immature cells)
  2. Recent acute loss of blood cell mass (i.e. bleeding or hemolysis), causing early bone marrow release of reticulocytes

Elevated (>2% of RBC count) with blood loss; hemolysis usually higher

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7
Q

Anemias

A

Types of anemia:
1. Aplastic anemia: bone marrow does not produce any blood cells

  1. Nutritional anemia: specific cellular abnormalities directly related to lack of nutrient
  2. Hemolytic anemia: inappropriate lysis of RBCs outside normal spleen/liver pathways
  3. Bone marrow dysfunction: inadequate stem cells or differentiation in marrow
  4. Blood loss
  5. Anemia of chronic illness: metabolic depletion of reserve and inability to replenish RBCs
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8
Q

Anemia: Signs and Symptoms

A

CV system (Compensatory mechanisms wrt low oxygen-carrying capability):

  1. Tachycardia
  2. Full, bounding pulses
  3. Cardiac murmurs
  4. HTN

CV system (Due to non-effective compensatory mechanisms or volume loss):

  1. Weak, thready pulses
  2. Hypotension
  3. Cool extremities

Neurological system:

  1. HA
  2. Confusion
  3. Cognitive impairment

Respiratory system:

  1. Tachypnea
  2. Dyspnea

GI/GU:

  1. Oliguria
  2. Constipation

Other S/S:

  1. Acidosis
  2. Hypothermia
  3. Fatigue
  4. Pallor
  5. Blood loss
  6. Bruising
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9
Q

Iron Deficiency Anemia

A

Iron deficiency is the most prevalent nutritional deficiency in the world

Related to:

  1. Chronic blood loss (i.e. Menstrual bleeding, CA, ulcerative colitis, PUD)
  2. Insufficient absorption (i.e. Crohn’s disease, celiac disease, PPIs and NSAID use)

“Hallmark” CMs:

  1. Pica: compulsion to eat non-food items (often resolved with iron repletion)
  2. Glossitis: painful, smooth, red tongue; cracks in corners of the mouth
  3. Koilonychias: spooning and thinning nails — due to blood flow abnormalities

Iron supplements are constipators (and can exacerbate anemia) — admin. with ascorbic acid and encourage fluid intake

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10
Q

Nutritional Anemia: Nursing Diagnosis & Interventions

A

Nursing diagnosis of patients with nutritional anemias:

  1. Inadequate tissue perfusion
  2. Fatigue
  3. Activity intolerance

Interventions & education of patients with nutritional anemias:

  1. Decrease/minimize blood loss
  2. Increase dietary iron (i.e. dark-green leafy greens, meats, iron-fortified cereal/bread)
  3. Increase dietary vitamin C (promotes iron absorption)
  4. Limit calcium supplements (interfere with iron absorption)
  5. Dietary supplements
  6. Report S/S of anemia: SOB, increased fatigue, and bleeding
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11
Q

Vitamin B12 Anemia

A

More likely to cause neurological and psychiatric dysfunction (related to demyelination of nerves)

“Hallmark” CMs of vitamin B12 anemia:

  1. Paresthesia: numbness and tingling in hands and feet
  2. Lhermitte sign: electric shock sensation with neck flexion
  3. Depression
  4. Impaired taste and balance
  5. Visual disturbances
  6. Tinnitus

Sources of vitamin B12:

  1. Meat
  2. Dairy
  3. Seafood
  4. Eggs
  5. B12 supplements (Oral and injection)
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12
Q

Folic Acid Anemia

A

Folate acid insufficiency is associated with:

  1. Gastric bypass surgery
  2. Whipple procedure (pancreatic CA surgery)
  3. Alcoholism — increased risk of pancytopenia (suppressed production of different cell types)
  4. Oral contraceptives
  5. Metformin
  6. Chemotherapy

Neurological symptoms: Confusion or disorientation (common)

Folic acid supplements are inducers of Phenytoin/Dilantin (increased risk of seizure breakthrough)

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13
Q

Nursing Care & Management of Patients with Anemia

A

Nursing care of patients with anemia:

  1. Balance physical activity, exercise, and rest
  2. Adequate nutritional support and supplemental admin. (i.e. iron, EPO, oxygenation)
  3. Blood transfusions

Management of patients with anemia:

  1. Ensure adequate safe perfusion
  2. IV fluids, blood transfusions, protein/coagulation factors, and crystalloid fluids admin.
  3. Remove underlying cause of exacerbation
  4. Reduce oxygen demands
  5. Bone marrow stimulants (EPO) admin. when Hgb <10 — Monitor for HTN and hyper-coagulability, and ensure adequate ferritin and iron precursors
  6. Immunosuppressives admin. if etiology of lysis is autoimmune
  7. Blood and marrow transplant (BMT)/Hematopoietic stem cell transplant (HSCT) if there is permanent stem cell damage
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14
Q

Blood Transfusion: Administration

A

Types of blood transfusion:

  1. Whole blood
  2. Packed RBCs
  3. FFP
  4. Platelets

Equipment:

  1. Normal Saline (always admin. with blood products)
  2. Blood tubing with/without filters

Timing:

  1. Patient timing
  2. Transfusion timing (wide open vs. over 3 hours)
  3. RN timing

Pre-Assessment:

  1. Lung sounds
  2. Skin
  3. Vitals

Checking blood (2 nurses):

  1. Consent for blood
  2. Patient ID
  3. Blood type of patient
  4. Blood type of product
  5. Blood ID number
  6. Expiration date
  7. Special preparations (neutrophils/irradiated)
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15
Q

Blood Transfusion: Signs and Symptoms of Reactions

A

ALLERGIC RXN:

  1. Facial flushing
  2. Hives/rash
  3. Anxiety
  4. Wheezing
  5. SOB
  6. Hypotension (histamines causes BVs to widen)

FEBRILE RXN:

  1. Fever
  2. Chills
  3. Anxiety
  4. HA
  5. Tachycardia
  6. Tachypnea

HEMOLYTIC RXN:

  1. Chest pain
  2. Hemoglobulinuria
  3. Lower back pain
  4. Fever
  5. Chills
  6. Tachycardia
  7. Hypotension
  8. Tachypnea
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16
Q

Blood Transfusion: Management

A

Preventing transfusion reactions:

  1. Monitoring
  2. Med. admin. prior to transfusion — i.e. Tylenol for fever; Benadryl for allergic reactions

Reaction management:

  1. Discontinue product and preserve tubing
  2. Normal saline admin.
  3. New type and crossmatch
  4. Coombs test — detects antibodies (identifies hemolytic reaction)
  5. Urine

Fluid overload management:

  1. Check lung sounds
  2. BP
  3. Weight gain
  4. Exercise intolerance
  5. Lasix admin.
17
Q

Sickle Cell Disease

A

An autosomal recessive (inherited) disease characterized by sickling of RBCs in the presence of hypoxemia due to abnormal Hgb S DNA structure

Sickled cells are longer and more stiff with a very shortened life span (20 days instead of normal 120 days)

Sickled cells easily hemolyze and destroy organs

Sickling of cells is intermittently triggered (there are few symptoms when not in crisis); there is some reversal of symptoms with correction of hypoxemia

18
Q

Sickle Cell Disease: Diagnosis

A

Sickle cell diagnosis:
1. CBC

  1. RBC indices
  2. Coagulation profile
  3. Chemistry tests
  4. Bilirubin
  5. Haptoglobin test (binds with heme)
  6. Transferrin saturation (binds with iron)
  7. Ferritin test (early iron precursor)
  8. Hgb electrophoresis: specific diagnosis that shows the presence of abnormal Hgb
19
Q

Sickle Cell Crisis: Signs and Symptoms

A

Hypoxemia is triggered by:

  1. Dehydration
  2. Cold temps.
  3. Infection
  4. Low atmospheric oxygen

Types of sickling crisis:
1. Vaso occlusion (most common) is triggered by hypoxemia; it causes tissue hypoxia and pain — S/S: Cool, cyanotic extremities, splenic infarction, stroke, and MI

  1. Aplastic
  2. Sequestration: excessive amount of blood becomes trapped in the spleen, causing hypovolemic shock
  3. Hemolytic
20
Q

Sickle Cell Disease: Joint Complications

A

Dactylitis (“Sausage digit” or Hand Foot Syndrome): severe pain that affects the bones of the hands and feet; it is often the first symptom of sickle cell disease between the time of birth and 4 yrs. of age

Swelling is caused by blocked blood circulation; S/S: Extreme pain, tenderness, swelling

21
Q

Sickle Cell Disease: Management

A

Primary treatment of sickle cell disease:

  1. Identify and avoid triggers
  2. Prevent hypoxemia
  3. Promote healthy lifestyle, nutrition, and sleep
  4. Limit sickling episodes

Management of sickle cell disease:

  1. Control hypoxemia (oxygen therapy admin.)
  2. Control thromboses (fluid admin.)
  3. Aggressively manage crisis-induced pain (rapid opioid admin.)
  4. Compensate for past hemolysis events
  5. Incentive spirometry — prevents pneumonia and atelectasis (due to inability to take deep breath)
  6. Supportive care — addresses challenges of exercise, limiting sickling, and chronic illness issues
  7. Minimize long-term organ dysfunction
22
Q

Sickle Cell Disease: Counseling

A

Pre-pregnancy counseling:

  1. Planning and anticipation
  2. Health insurance
  3. Parental testing

Parental counseling:

  1. Infant testing
  2. Health care planning
  3. Development
  4. Psychologic challenges
23
Q

Normal Clotting Cascade

A

Clotting cascade pathway:
1. Clotting stimulus (i.e. Tissue injury, vessel injury, FB in bloodstream)

  1. Vasoconstriction (immediate); serotonin release
  2. Platelet plug: one of the early phases of establishing a clot (2-5 hours); ADP release
  3. Fibrin clot formation (1-3 days); plasminogen activated
  4. Fibrinolysis
24
Q

Medications that Commonly Cause Anemia and Thrombocytopenia

A

Anticoagulants:

  1. Warfarin (Coumadin)
  2. Heparin
  3. Lovenox

Fibrinolytics: Alteplase

Platelet inhibitors: Plavix

NSAIDs

Drugs that interfere with platelet production and function:

  1. Antibiotics
  2. Thiazide diuretics
  3. Quinidine
  4. Sulfonamides

Drugs that interfere with clotting factors:

  1. Amiodarone
  2. Anabolic steroids
  3. Warfarin (Coumadin)
  4. Heparin

Drugs that decrease vitamin K:

  1. Antibiotics
  2. Clofibrate
25
Q

Thrombocytopenia

A

Low blood platelet count; it is not a disease, but a complication or syndrome

Common etiologies:

  1. Bone marrow disease
  2. Chemical exposure (i.e. Insecticides and dry cleaning chemicals)
  3. Meds. (i.e. Heparin)
  4. Radiation exposure
  5. Splenic disease
  6. Hypo/hyperthermia
  7. Large indwelling venous catheters
  8. Hemorrhagic conditions — i.e. Disseminated intravascular coagulation (DIC): over activation of proteins that control blood clotting (can lead to massive bleeding in other places)
26
Q

Assessment of Patients with Platelet Disorders

A

Patient & FHX:

  1. Unusual bleeding with injury
  2. Liver disease
  3. GI disease
  4. Alcohol or drug use
  5. Occupation
  6. Viral illness
  7. Meds.

Physical exam:

  1. Bruising
  2. Jaundice
  3. Soft tissue bleeding (i.e. Bruising, petechiae)
  4. Mucosal bleeding (i.e. Gum bleeding, hematuria, fecal occult blood)

Diagnostic studies:

  1. Mild (PLT count <50,000); Moderate (<20,000); Severe (<10,000)
  2. Platelet quality — bleeding time
27
Q

Thrombocytopenia: Management

A

Management of patients with thrombocytopenia:
1. Remove cause of thrombocytopenia

  1. Glucocorticoid admin. — temporarily suppresses the body’s immune system, slowing platelet destruction
  2. Platelet transfusions (more reactions than RBC transfusions) — Fewer donors reduce risk of reactions (ideal if bone marrow transplant is later required)
  3. Bone marrow growth factors (i.e. Oprelvekin, neumega) admin.
  4. Anti-thrombolytic therapy (i.e. Aminocaproic acid/Amicar) — does not correct platelet abnormality (it is supportive)
  5. Immunosuppressives admin. — helpful if etiology of lysis is immunologic
  6. Splenectomy (extreme cases)
28
Q

Thrombocytopenia: Nursing Management

A

Nursing management of patients with thrombocytopenia:
1. Assess all excrement for visual blood

  1. Visualize orifices/skin/mucosa for bleeding
  2. Reduce risk of bleeding — i.e. Elevating HOB, avoiding constipation, fall precautions, applying pressure after invasive procedures, and avoiding IM injections
  3. Med admin. to prevent clot breakdown
  4. Platelet transfusions
  5. Monitor for excessive blood loss (i.e. BP, tachycardia, pallor, diaphoretic)
  6. Minimize automatic BP cuff use

Chronic Alterations: Exam 1 (5 decks)

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