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9 Hematology.

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Presentation on theme: "9 Hematology."— Presentation transcript:

1 9 Hematology

2 Multimedia Directory Slide 71 Blood Type Animation
Slide 111 Sickle Cell Anemia Animation

3 Standard Medicine (Hematology)

4 Competency Integrates assessment findings with principles of epidemiology and pathophysiology to formulate a field impression and implement a comprehensive treatment/disposition plan for a patient with a medical complaint.

5 Introduction Hematology: study of blood and blood-forming organs.
Hematologic disorders: Red blood cell disorders White blood cell disorders Platelet disorders Coagulation problems

6 Introduction Some hematologic diseases genetic in origin
Hemophilia A classic example. Some hematologic diseases more common in certain ethnic groups. Sickle cell anemia among African Americans.

7 Introduction Hematologic disorders may predispose patients to infection and intolerance to exercise, hypoxia, acidosis, blood loss. Careful examination and history taking necessary to clarify diagnosis. Often laboratory findings will be needed to confirm diagnosis.

8 Anatomy, Physiology, and Pathophysiology
Hematopoietic system consists of: Blood (both cells and plasma) Bone marrow Liver Spleen Kidneys Teaching Tips It's helpful to review the immune system and its components prior to discussion of the hematopoietic system, as they have many components that are shared.

9 Anatomy, Physiology, and Pathophysiology
Cellular components of blood formed by differentiation of pluripotent stem cells (hematopoiesis). Stem cells reproduce to maintain constant population of cells. Mature into basophils, eosinophils, neutrophils, monocytes, erythrocytes, thrombocytes.

10 Anatomy, Physiology, and Pathophysiology
Kidneys (lesser extent liver) produce erythropoietin (hormone responsible for red blood cell production). Liver removes toxins from blood and produces many clotting factors and proteins in plasma. Spleen has cells that scavenge abnormal blood cells and bacteria.

11 Anatomy, Physiology, and Pathophysiology
Blood volume relatively constant at about 6% of total body weight. Determinants of blood volume: red cell mass and plasma volume. Red blood cells remain in intravascular compartment. Only changes in rate of production can alter size of circulating red cell mass.

12 Anatomy, Physiology, and Pathophysiology
Plasma volume can rapidly change due to fluid shifts between intravascular and extravascular space. Helps to preserve circulating blood volume in event of acute hemorrhage.

13 Anatomy, Physiology, and Pathophysiology
Other compensatory mechanisms: Vasoconstriction Tachycardia Increased cardiac contractility When compensatory measures fail, patient enters decompensated shock.

14 Anatomy, Physiology, and Pathophysiology
Components of Blood Plasma: thick, pale-yellow fluid; 90–92% water; 6–7% proteins. Plasma transports cellular components of blood and dissolved nutrients throughout body. It also transports waste products from cellular metabolism to liver, kidneys, lungs, where removed from body.

15 Anatomy, Physiology, and Pathophysiology
Components of Blood Most plasma components can move back and forth across capillary membranes to interstitial fluid. Plasma proteins have great difficulty diffusing across membranes. Remain in plasma to help retain water in capillaries (osmotic pull, or oncotic pressure).

16 Anatomy, Physiology, and Pathophysiology
Components of Blood Plasma proteins' other functions: Clotting of blood Dismantling of clots Buffering of blood's acid-base balance Transporting hormones and regulating their effects Providing source of energy

17 Anatomy, Physiology, and Pathophysiology
Components of Blood Electrolytes found in plasma. Chemical substances that dissociate into charged particles in water. Essential for nerve conduction, muscle contraction, water balance.

18 Anatomy, Physiology, and Pathophysiology
Components of Blood Carbohydrates in plasma in form of glucose; primary energy source. Plasma performs role in gas transport. Carbon dioxide and oxygen dissolved and transported in plasma.

19 Anatomy, Physiology, and Pathophysiology
Components of Blood Red blood cells: transport oxygen from lungs to tissues. Red blood cell (RBC), or erythrocyte: biconcave disc; does not have nucleus when mature. Contains hemoglobin molecules that transport oxygen.

20 Scanning electron photomicrograph of red blood cells moving through a blood vessel. (Centers for Disease Control/Janice Haney Carr)

21 Anatomy, Physiology, and Pathophysiology
Components of Blood Oxygen transport   Greater number of red blood cells, greater potential oxygen-carrying capacity. Percentage of oxygen bound to hemoglobin increases as PO2 increases. Normal PO2 95–100 mmHg.

22 Anatomy, Physiology, and Pathophysiology
Components of Blood Oxygen transport  Hemoglobin has affinity for oxygen. The lower the pH, the more readily hemoglobin will release oxygen. Bohr effect: waste CO2 from tissues diffuses into blood, causing hemoglobin to give up more oxygen to tissues.

23 Anatomy, Physiology, and Pathophysiology
Components of Blood Oxygen transport Except for hemoglobin, most abundant chemical in red blood cells is 2,3-bisphosphoglycerate (2,3-BPG). During prolonged periods of hypoxia, level of 2,3-BPG increases. Increased 2,3-BPG makes it difficult for oxygen to combine with hemoglobin in lungs.

24 Anatomy, Physiology, and Pathophysiology
Components of Blood Oxygen transport Rise in body temperature causes decrease in hemoglobin's affinity for oxygen. Exercise: decrease in pH and increase in body temperature causes hemoglobin to release oxygen.

25 Anatomy, Physiology, and Pathophysiology
Components of Blood Oxygen transport The greater the substance's affinity for binding sites, the more readily substance will bind with hemoglobin. Carbon monoxide has 210–250 times oxygen's affinity for hemoglobin and competes for same binding sites.

26 Anatomy, Physiology, and Pathophysiology
Components of Blood Erythropoiesis: red blood cell production. Erythropoietin (hormone produced by kidney): stimulates bone marrow's production of erythrocytes. RBC lives approximately 120 days.

27 Anatomy, Physiology, and Pathophysiology
Components of Blood Hemorrhage, hemolysis (destruction of the RBC), or sequestration of RBCs by liver or spleen may significantly reduce their life span. Hemorrhage may occur outside body or be hidden within body cavity, such as in peritoneum, retroperitoneum, gastrointestinal (GI) tract.

28 Anatomy, Physiology, and Pathophysiology
Components of Blood Hemolysis may occur within circulatory system in sickle cell disease and rare autoimmune anemias. Spleen and liver contain scavenger cells called macrophages; remove damaged or abnormal RBCs from circulation.

29 Anatomy, Physiology, and Pathophysiology
Components of Blood RBCs quantified or measured and reported in two ways: red blood cell count and hematocrit. RBC count: total number of RBCs reported in millions per cubic millimeter (mm3) of blood.

30 Anatomy, Physiology, and Pathophysiology
Components of Blood Hematocrit: packed cell volume of red blood cells per unit of blood. Measurement obtained by placing sample of blood in centrifuge and spinning it at high speed so that cellular elements separate from plasma.

31 Anatomy, Physiology, and Pathophysiology
Components of Blood Hematocrit: red blood cells heaviest because they carry iron-containing pigment hemoglobin; forced to bottom of tube. Above red blood cells are white blood cells; on top specimen is plasma. Normal values range between 40 and 52%.

32 Hematocrit, including plasma.

33 Anatomy, Physiology, and Pathophysiology
Components of Blood Measure concentration of hemoglobin present; number of grams of hemoglobin present per deciliter of whole blood. Common to measure hemoglobin in addition to hematocrit (H&H). Both values indicate RBC volume and capability.

34 Anatomy, Physiology, and Pathophysiology
Components of Blood White blood cells (WBCs; leukocytes or white corpuscles): circulate through bloodstream and tissues, providing protection from foreign invasion. Marginated leukocytes do not move freely within bloodstream; attach to blood vessels' walls.

35 Anatomy, Physiology, and Pathophysiology
Components of Blood Demargination: marginated leukocytes return to circulation in response to stress, corticosteroids, seizures, epinephrine, exercise. Chemical signals (chemotaxis). WBCs engulf and destroy invader by phagocytosis.

36 White blood cells engulfing and destroying an invader in the process called phagocytosis.

37 Anatomy, Physiology, and Pathophysiology
Components of Blood Healthy people have 5,000 to 9,000 WBCs per microliter of blood. Infection can increase number to more than 16,000 WBCs. Increase in WBC number classic sign of bacterial infection.

38 Anatomy, Physiology, and Pathophysiology
Components of Blood WBCs originate in bone marrow from undifferentiated stem cells. Leukopoiesis: stem cells respond to growth factors that allow them to differentiate into three blasts: myeloblasts, monoblasts, lymphoblasts.

39 Anatomy, Physiology, and Pathophysiology
Components of Blood WBCs categorized as granulocytes, monocytes, lymphocytes. Granulocytes: classified by type of stain they absorb. Basophils: absorb basic stains; blue granules. Eosinophils: absorb acidic stains; red granules.

40 Anatomy, Physiology, and Pathophysiology
Components of Blood Granulocytes: classified by type of stain they absorb. Neutrophils: absorb neither acidic nor basic stains well; pale blue and pink granules.

41 Anatomy, Physiology, and Pathophysiology
Components of Blood Basophils: function in allergic reactions. Store histamine; contain heparin, which breaks down blood clots. Eosinophils: inactivate chemical mediators of acute allergic reactions. Contain major basic protein (MBP), which fights parasitic infections.

42 Anatomy, Physiology, and Pathophysiology
Components of Blood Neutrophils: function to fight infection. Engulf and kill microorganisms that invade body. If neutrophil count low (neutropenia), body cannot mount appropriate response to infection.

43 Anatomy, Physiology, and Pathophysiology
Components of Blood Monocytes Macrophages ("garbage collectors" of immune system) engulf both foreign invaders and dead neutrophils. Monocytes and macrophages secrete growth factors to stimulate production of granulocytes and red blood cells.

44 Anatomy, Physiology, and Pathophysiology
Components of Blood Lymphocytes Primary cells involved in body's immune response. Located throughout body in circulating blood and in tissues. Small, round, white blood cells containing no granules on staining.

45 Anatomy, Physiology, and Pathophysiology
Components of Blood Immunity Two basic subpopulations of lymphocytes: T cells and B cells. T cells: responsible for developing cell-mediated, or cellular, immunity. B cells: produce antibodies to combat infection (humoral immunity).

46 Anatomy, Physiology, and Pathophysiology
Components of Blood Autoimmune disease Body makes antibodies against its own tissues. May be limited to specific organs or involve virtually every tissue type. Genetic factors and viral infections.

47 Anatomy, Physiology, and Pathophysiology
Components of Blood Alterations in immune response  Organ transplant patients must take drugs that inhibit cellular immunity and prevent graft rejection. If they do not, T cells will recognize new organ as "not self" and begin attacking it; called rejection. 

48 Anatomy, Physiology, and Pathophysiology
Components of Blood Alterations in immune response  Human immunodeficiency virus (HIV) destroys cell-mediated immunity by selectively attacking and killing T cells. Cancer patients often immunocompromised by disease itself or chemotherapy agents that attack bone marrow.

49 Anatomy, Physiology, and Pathophysiology
Components of Blood Inflammatory process Nonspecific defense mechanism; wards off damage from microorganisms or trauma. Causes: infectious agent, trauma, chemical, immunologic. Results in redness, warmth, swelling, usually pain and fever.

50 Anatomy, Physiology, and Pathophysiology
Components of Blood Platelets, or thrombocytes Small fragments of large cells called megakaryocytes. Platelets from 150,000 to 450,000 per microliter of blood. Form plug at initial bleeding site; secrete factors important in clot formation.

51 Anatomy, Physiology, and Pathophysiology
Components of Blood Platelets, or thrombocytes Too few platelets (thrombocytopenia) can lead to bleeding problems and blood loss. Too many platelets (thrombocytosis) may cause abnormal clotting, plugs in vessels, and emboli that may travel to extremities, heart, lungs, brain.

52 Anatomy, Physiology, and Pathophysiology
Components of Blood Platelets, or thrombocytes Survive 7 to 10 days; removed from circulation by spleen. Activated when they contact injured tissue. As platelets aggregate, they release chemical messengers that activate blood clotting system.

53 Anatomy, Physiology, and Pathophysiology
Hemostasis Combined three mechanisms that work to prevent or control blood loss: Vascular spasms Platelet plugs Stable fibrin blood clots (coagulation)

54 Anatomy, Physiology, and Pathophysiology
Hemostasis When blood vessel tears, smooth muscle fibers in vessel walls contract. Causes vasoconstriction and reduces size of tear. Less blood flows through constricted area, limiting blood loss. Smaller tear makes it easier for platelet plug to develop and stop blood loss.

55 Anatomy, Physiology, and Pathophysiology
Hemostasis At any tear in blood vessel, platelets aggregate and adhere to collagen (connective tissue that supports blood vessels). Forms platelet plug. Formation of stable fibrin clot (blood coagulation) initiated by platelet plug.

56 Illustration of clot formation.

57 Anatomy, Physiology, and Pathophysiology
Hemostasis Damage to cells or to vessel lining, starts coagulation cascade. Sequence of events can be activated either by damage to vessels or by trauma to blood from turbulence. Either results in cascade's progression to clot.

58 Anatomy, Physiology, and Pathophysiology
Hemostasis Most clotting proteins produced in liver; circulate in inactive state (prothrombin and fibrinogen). Damaged cells send out chemical message; activates specific clotting factor. Activates each protein in turn until stable fibrin clot forms.

59 Anatomy, Physiology, and Pathophysiology
Hemostasis To completely stop bleeding, coagulation cascade relies on platelet plug and clotting factors to interact. Once bleeding stops, inflammatory and healing processes can begin. Class Activities Have students diagram the clotting cascade. Have them demonstrate how it progresses and at which point each component is involved.

60 The coagulation cascade.

61 Anatomy, Physiology, and Pathophysiology
Hemostasis Development of clot does not end coagulation cascade. Dismantling (lysing) of clot through fibrinolysis; takes from hours to days. By that time, scarring has begun.

62 Anatomy, Physiology, and Pathophysiology
Hemostasis Thrombosis (clot formation), when in coronary arteries or cerebral vasculature, may lead to heart attack and stroke. Fibrinolytics effective only against blockages whose components include fibrin clot.

63 Anatomy, Physiology, and Pathophysiology
Hemostasis Patients who lack clotting factors can have bleeding disorders. Patients who take medications that decrease effectiveness of platelets or coagulation cascade may have bleeding problems. Both may complicate assessment and treatment.

64 Anatomy, Physiology, and Pathophysiology
Hemostasis Medications examples: Aspirin Dipyridamole (Persantine) Ticlopidine (Ticlid) Heparin Warfarin (Coumadin)

65 Anatomy, Physiology, and Pathophysiology
Hemostasis Glycoprotein IIb/IIIa receptors on platelet membrane; major platelet surface receptor involved in final pathway of platelet aggregation. Treat acute coronary syndrome, often in combination with angioplasty with or without stent placement.

66 Anatomy, Physiology, and Pathophysiology
Hemostasis Glycoprotein IIb/IIIa inhibitors classified as potent platelet inhibitors. Abciximab (ReoPro) Eptifibatide (Integrilin) Tirofiban (Aggrastat)

67 Anatomy, Physiology, and Pathophysiology
Hemostasis All below may lead to increased clotting: Vitamin K (AquaMEPHYTON) Relative or complete immobility Trauma Polycythemia Cancer By-products of tobacco use

68 Anatomy, Physiology, and Pathophysiology
Blood Products and Blood Typing Blood transfusion: transplantation of blood or component of blood from one person to another. Accomplished by IV infusion. Various types of transfusions given for various purposes. Knowledge Application Some areas allow paramedics to give blood infusions. If your area is one, how does this affect your treatment of bleeding disorders and trauma? What are the methods of storing the blood? What blood type is used?

69 Anatomy, Physiology, and Pathophysiology
Blood Products and Blood Typing Blood type A: A antigens on RBCs; anti-B antibodies. Blood type B: B antigens on RBCs; anti-A antibodies. Blood type AB: RBCs have both antigens, but neither antibody. Blood type O: neither antigen, but both antibodies.

70 Anatomy, Physiology, and Pathophysiology
Blood Products and Blood Typing Blood type inherited trait. Type AB blood: universal recipient. Type O blood: universal donor. Crossmatching blood: checking samples from both donor and recipient to ensure greatest compatibility.

71 Click here to view an animation on the topic of blood types.
Blood Type Animation Questions: Explain how blood types were first discovered. List the four major blood types. Why is type O considered the universal donor? Why is type AB considered the universal recipient? What blood type could be given to a trauma patient who needs blood before a type and screen can be run? Click here to view an animation on the topic of blood types. Back to Directory

72 Anatomy, Physiology, and Pathophysiology
Blood Products and Blood Typing Rh factor: antigen with possible severe hemolytic reaction. Rh positive: person has Rh factor. Rh negative: person does not have Rh factor. Erythroblastosis fetalis (hemolytic disease of newborn): can lead to fatal hemolytic Rh reaction in neonates.

73 Anatomy, Physiology, and Pathophysiology
Transfusion Reactions Hemolytic transfusion reaction: donor's and recipient's blood not compatible. Signs and symptoms: facial flushing, hyperventilation, tachycardia, sense of dread, hives, chest pain, wheezing, fever, chills, cyanosis, flank pain.

74 Anatomy, Physiology, and Pathophysiology
Transfusion Reactions Stop transfusion immediately. Change IV tubing; IV therapy normal saline or lactated Ringer's solution. Administer bolus as necessary. Furosemide (Lasix) administered to promote diuresis. In extreme cases of anaphylactic reaction, administer IV epinephrine.

75 Anatomy, Physiology, and Pathophysiology
Transfusion Reactions Most common transfusion reaction is febrile nonhemolytic reaction. Sensitization to antigens on white blood cells, platelets, plasma proteins. Signs and symptoms: headache, fever, chills. Always stop transfusion before attempting to treat it.

76 Anatomy, Physiology, and Pathophysiology
Transfusion Reactions Change all tubing. Initiate normal saline IV. Diphenhydramine (Benadryl) and antipyretic (ibuprofen, acetaminophen) for fever. In event of any transfusion reaction, return all blood bags, tubing, filters to blood bank for analysis.

77 Anatomy, Physiology, and Pathophysiology
Transfusion Reactions Blood transfusion adds fluid to system. Patient may experience signs and symptoms of circulatory overload. Same as those for left ventricular failure; pulmonary edema, dyspnea, chest pain. Hypotension not usually problem.

78 General Assessment and Management
Patients with infection, WBC abnormalities, or transfusion reactions may present with febrile symptoms. May develop hemodynamic instability. Acute hemodynamic compromise found in patients with anemia secondary to acute blood loss, coagulation defects, autoimmune disease.

79 General Assessment and Management
Treatment of patients with disorders of hematopoietic system is supportive. Recognize need for rapid transport in patients with hemodynamic instability. May require transfusion or other definitive care measures. Always contact medical direction for questions or problems. Teaching Tips These types of patients should be integrated into your medical patient assessment practices.

80 General Assessment and Management
Perform scene size-up; take Standard Precautions. Primary assessment for life threats. Determine responsiveness; assess airway, breathing, circulation. Alterations in hematopoietic system may present as life-threatening bleeds or overwhelming infections with septic shock.

81 General Assessment and Management
Do not spend time obtaining complete set of vital signs during primary assessment. Check ABCs; quickly determine priority for transport. Critical or unstable patients candidates for expeditious transport.

82 General Assessment and Management
Complete secondary assessment. Trauma patients and unresponsive medical patients often present life-threatening problems; noted in primary assessment. For responsive medical patient, obtain SAMPLE history; perform physical exam.

83 General Assessment and Management
Obtain set of vital signs; place pulse oximeter. Ask for chief complaint; attention to generalized complaints. Note dyspnea, palpitations, dizziness with changes in patient's position. Patients with hematologic problems may suffer syncope.

84 General Assessment and Management
Bleeding abnormalities may be disguised as gastrointestinal upset. Ask about overt bleeding with vomiting or diarrhea. Atraumatic bleeding of gums almost always points to underlying hematologic abnormality. Ask about changes in urination, hematuria, menstrual pattern.

85 General Assessment and Management
Determine any allergies. Make note of all of patient's medications and compliance. Ask about past medical history. Ask about bloodborne infections. Family history: hemophilia, sickle cell disease, cancer, or death at early age not trauma related.

86 General Assessment and Management
Inquire about social habits. Last oral intake and unusual events. If history suggests hematopoietic problem, look for potential pathology during physical exam.

87 General Assessment and Management
Nervous System Determine level of consciousness using AVPU system. Complaint of being "weak and dizzy." Associated with possible anemia. Determine whether patient had syncopal episode. Always examine eyes for abnormalities.

88 General Assessment and Management
Skin Jaundice (yellow skin): liver disease or hemolysis of RBCs. Florid (reddish) appearance associated with polycythemia. Anemia typically exhibits pallor. Petechiae (tiny red dots on skin).

89 Jaundice. (© Edward T. Dickinson, MD)

90 General Assessment and Management
Skin Purpura (large purplish blotches related to multiple hemorrhages into skin). Bruising. Inquire about pruritus (itching).

91 (a) Petechiae; (b) purpura.

92 General Assessment and Management
Lymphatic Affected early in hematopoietic diseases, especially those of immune system. Pay particular attention to lymph nodes; note any enlargement; compare sides.

93 General Assessment and Management
Gastrointestinal Epistaxis (nosebleed) common. Patients may swallow great deal of blood; become nauseated. Blood acts as cathartic (laxative). Patients who swallow moderate amounts of blood report loose bowel movements. Often dark (melena); blood bright red or appears like coffee grounds.

94 General Assessment and Management
Gastrointestinal Bleeding of gums early findings of hematologic problems; note presence of gingivitis. Liver disease can slow blood clotting. As liver fails, bilirubin level will increase, resulting in jaundice. Problems with spleen, liver, or both can lead to abdominal pain.

95 General Assessment and Management
Gastrointestinal Splenomegaly common in hematologic problems. Spleen can become markedly enlarged. Patients with sickle cell anemia will often develop splenic infarcts.

96 General Assessment and Management
Musculoskeletal Many hematopoietic problems autoimmune in nature. Rheumatoid arthritis: body's immune system attacking tissues in joints. Patients with blood clotting disorders such as hemophilia will often develop hemarthrosis (bleeding into joint).

97 General Assessment and Management
Cardiorespiratory Patients with anemia often develop dyspnea, tachycardia, chest pain. In severe cases, develop high-output heart failure to compensate for profound anemia. Always auscultate for breath sounds; note crackles or rhonchi indicative of heart problems or infection.

98 General Assessment and Management
Genitourinary Due to bleeding disorders or infection. Bleeding disorders can cause: Hematuria (blood in urine) Blood in scrotal sac in males Menorrhagia (heavy menstrual bleeding) Frank vaginal bleeding (dysfunctional uterine bleeding)

99 General Assessment and Management
Genitourinary Immunocompromised patients at increased risk for developing infections. Sickle cell anemia can cause priapism.

100 General Assessment and Management
General Management of Hematopoietic Emergencies Place on high-concentration supplemental oxygen; monitor breathing for difficulty or fatigue. Be ready to assist ventilations with bag-valve mask. Assess circulatory system.

101 General Assessment and Management
General Management of Hematopoietic Emergencies Consider fluid volume replacement. Be alert for arrhythmias; treat accordingly. Create optimum environment for blood to perform its tasks of oxygen delivery and waste product removal.

102 General Assessment and Management
General Management of Hematopoietic Emergencies Transport to appropriate facility. Provide comfort measures: analgesia. Provide psychological support to both patient and family.

103 Managing Specific Patient Problems
Diseases of the Red Blood Cells RBC diseases: too many, too few, or improperly functioning RBCs. Polycythemia: excess of RBCs. Anemia: inadequate number of red blood cells; inadequate hemoglobin within RBCs. Knowledge Application Many of the disorders discussed are non-acute and secondary to other more life-threatening problems. How do these problems compound other issues your patient might have? Which ones are more likely to become very unstable?

104 Managing Specific Patient Problems
Diseases of the Red Blood Cells Anemia Classified as hematocrit of less than 37% in women; less than 40% in men. Due to reduction in number of RBCs cells or amount or quality of hemoglobin in RBCs.

105 Managing Specific Patient Problems
Diseases of the Red Blood Cells Anemia Sign of underlying disease process. Blood loss (acute or chronic) can cause anemia. Can be self-limiting disease or lifelong illness requiring periodic transfusions. Hemolytic anemia: destruction of RBCs; hereditary or acquired.

106 Managing Specific Patient Problems
Diseases of the Red Blood Cells Anemia Acquired hemolytic anemias: immune system disorders, drug effects, environmental effects. Anemias caused by inadequate RBC production: iron deficiency anemia, pernicious anemia, anemia of chronic disease.

107 Managing Specific Patient Problems
Diseases of the Red Blood Cells Anemia Sign, not disease process in itself. Results in hypoxia. Chronic anemias: pica, headache, dizziness, ringing in ears, irritability or difficulty concentrating, pallor, tachycardia. Angina pectoris important indicator.

108 Managing Specific Patient Problems
Diseases of the Red Blood Cells Anemia If develops rapidly, body does not have time to compensate for change; signs and symptoms of shock. If onset slower, body can adjust to reduced availability of oxygen. Treat hypoxia with supplemental oxygen. Avoid hyperoxia.

109 Managing Specific Patient Problems
Diseases of the Red Blood Cells Sickle cell disease (sickle cell anemia) Disorder of RBC production. Abnormal chemical sequence that gives red blood cells C, or sickle, shape when oxygen levels are low. Chronic anemia; results from destruction of abnormal RBCs. Discussion Topics Do any of these particular problems impact your transport decisions? What types of local facilities can manage these types of patients?

110 Scanning electron photomicrograph of sickle cells
Scanning electron photomicrograph of sickle cells. (Centers for Disease Control/Janice Haney Carr)

111 Sickle Cell Anemia Animation
Questions: Describe sickle cell anemia. What race is most at risk for sickle cell anemia? Describe the signs and symptoms of a sickle cell crisis. How is a sickle cell crisis managed in the prehospital setting? Click here to view an animation on the topic of sickle cell anemia. Back to Directory

112 Managing Specific Patient Problems
Diseases of the Red Blood Cells Sickle cell disease (sickle cell anemia) Average life span of sickled RBCs 10–20 days; 120 days for normal RBCs. Blockage of blood flow to tissues and organs common; following period of stress. This process (vasoocclusive crisis) characteristic of sickle cell anemia.

113 Managing Specific Patient Problems
Diseases of the Red Blood Cells Sickle cell disease (sickle cell anemia) Adult sickle cell patients have multiple organ problems. Disease inherited; primarily affects African Americans. Vasoocclusive crises: musculoskeletal and abdominal pain, priapism, pulmonary problems, renal crises, central nervous system (CNS) crises.

114 Managing Specific Patient Problems
Diseases of the Red Blood Cells Sickle cell disease (sickle cell anemia) Hematologic crises: fall in hemoglobin level, sequestration of RBCs in spleen, problems with bone marrow function. Infectious crises: functionally immunosuppressed; vulnerable to encapsulated bacteria.

115 Managing Specific Patient Problems
Diseases of the Red Blood Cells Sickle cell disease (sickle cell anemia) Prehospital primarily supportive. High-concentration oxygen to saturate as much hemoglobin as possible. IV therapy with isotonic crystalloid solution. May require large amounts of narcotics for pain control.

116 Managing Specific Patient Problems
Diseases of the White Blood Cells Result from too few WBCs (leukopenia), too many WBCs (leukocytosis), or improper WBC function. Reduction in number of neutrophils (neutropenia) predisposes patient to bacterial and fungal infections.

117 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukopenia/neutropenia Normal WBC count from 5,000 to 9,000 per cubic millimeter of blood. Absolute neutrophil count better indicator of immune system's status. Prehospital treatment supportive.

118 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukocytosis Increase in number of circulating white blood cells. Body exposed to infectious agent or particularly stressed. WBC count 10,800 to 23,000 per cubic millimeter of blood characteristic of bacterial infection.

119 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukocytosis Causes: bacterial infection, rheumatoid arthritis, diabetic ketoacidosis (DKA), leukemia, pain, exercise. Any patient with significantly elevated WBC count should be evaluated for possible leukemia.

120 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukemias Cancers of hematopoietic cells. Acute lymphocytic leukemia (ALL) Acute myelogenous leukemia (AML) Chronic lymphocytic leukemia (CLL) Chronic myelogenous leukemia (CML) Hairy cell leukemia

121 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukemias Chemotherapy, radiation therapy, bone marrow transplantation have resulted in cures of certain types. Deaths secondary to infection/bleeding. Signs and symptoms vary; moderate to severe anemia.

122 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukemias Many patients present with bleeding; due to thrombocytopenia. Patients will appear acutely ill. Prehospital treatment primarily supportive. Place in position of comfort. Administer supplemental oxygen.

123 Managing Specific Patient Problems
Diseases of the White Blood Cells Leukemias IV with isotonic crystalloid solution. Consider fluid bolus if dehydrated. Consider administration of analgesic. Increased risk of developing infection; employ proper isolation techniques.

124 Managing Specific Patient Problems
Diseases of the White Blood Cells Lymphomas Cancers of lymphatic system. Malignant lymphoma classified: Hodgkin's lymphoma Non-Hodgkin's lymphoma Long-term survival rate better with Hodgkin's lymphoma.

125 Managing Specific Patient Problems
Diseases of the White Blood Cells Lymphomas Presenting sign of non-Hodgkin's lymphoma: painless swelling of lymph nodes. Fever, night sweats, anorexia, weight loss, fatigue, pruritus. Treat patients with lymphomas symptomatically.

126 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Thrombocytosis: increase in number of platelets; due to increased platelet production. Most patients asymptomatic; prehospital treatment supportive.

127 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Thrombocytopenia: abnormal decrease in number of platelets. Due to decreased platelet production, sequestration of platelets in spleen, destruction of platelets, or any combination of the three.

128 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Acute idiopathic thrombocytopenia purpura (ITP): destruction of platelets by immune system. Most commonly seen in children following viral infection. Prehospital treatment supportive.

129 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Hemophilia: blood disorder; one of the proteins necessary for blood clotting missing or defective. Deficiency of factor VIII: hemophilia A. Deficiency of factor IX: hemophilia B (Christmas disease).

130 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Hemophilia Hemophilia A most common inherited disorder of hemostasis. Hemophilia B more rare; more severe. When injured, bleeding will take longer to stop; body cannot form stable fibrin clots.

131 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Hemophilia Occasionally life-threatening bleeds. Sex-linked, inherited bleeding disorder. Numerous bruises, deep muscle bleeding, joint bleeding called hemarthrosis.

132 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Hemophilia Most patients aware of diagnosis will tell you; Medic-Alert bracelets or similar devices. Prehospital treatment comprehensive. Be attentive to prolonged bleeding or possible rebleeds.

133 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities Hemophilia Administer supplemental oxygen. IV therapy with isotonic crystalloid. Be careful to prevent additional trauma. If joint injury with hemarthrosis, splinting extremity will sometimes help control pain.

134 Managing Specific Patient Problems
Diseases of the Platelets/Blood Clotting Abnormalities von Willebrand's disease Component of factor VIII deficient. In addition to clotting problem, platelet function abnormal. Disease inherited; not sex linked. Excessive bleeding, primarily after surgery or injury.

135 Managing Specific Patient Problems
Other Hematopoietic Disorders Disseminated intravascular coagulation (DIC) (consumption coagulopathy): disorder of coagulation caused by systemic activation of coagulation cascade. Bleeding most frequent sign; due to reduced fibrinogen level, consumption of coagulation factors, thrombocytopenia.

136 Managing Specific Patient Problems
Other Hematopoietic Disorders Disseminated intravascular coagulation Disease is quite grave. Oozing blood at venipuncture and wound sites; purpuric rash. Prehospital care symptomatic. Administration of fresh frozen plasma and platelets.

137 Managing Specific Patient Problems
Other Hematopoietic Disorders Multiple myeloma: cancerous disorder of plasma cells. Rarely found in persons under 40. Change or mutation in plasma cell in bone marrow. Cancerous cells crowd out healthy cells; reduction in blood cell production.

138 Managing Specific Patient Problems
Other Hematopoietic Disorders Multiple myeloma Patient becomes anemic; prone to infection. First sign is pain in back or ribs. Treatment: chemotherapy, radiation, bone marrow transplants. Prehospital care is supportive.

139 Managing Specific Patient Problems
Other Hematopoietic Disorders Multiple myeloma Establish IV of isotonic crystalloid solution. Consider fluid bolus if symptoms of dehydration. Consider analgesics if pain severe.

140 Summary Hematology is study of blood and blood-forming organs.
Blood consists of a liquid portion, or plasma, and formed elements—red blood cells, white blood cells, platelets.

141 Summary Each component of blood has various functions intrinsic to sustaining homeostasis. Red blood cells, composed of hemoglobin, transport oxygen to body tissues and remove wastes such as carbon dioxide.

142 Summary Plasma draws water into capillaries; assists in clotting blood, dismantling clots, buffering blood's acid-base balance, transporting hormones and regulating their effects, providing source of energy.

143 Summary White blood cells protect body from foreign invasion through processes of chemotaxis and phagocytosis. Platelets travel to site of damaged tissue and help to prevent blood loss.

144 Summary Hemostasis is body's way of preventing or controlling blood loss. Three phases of hemostasis: Vascular spasm Development of platelet plug Formation of stable fibrin clot (blood coagulation)

145 Summary Some diseases interfere with aspects of hemostasis; people who have these diseases may incur life-threatening hemorrhages from minor injuries. As a paramedic, you must understand hematology; breakdowns in hematologic system can complicate patient assessment and care.


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