Frank MacDonald RN, MN



UNIT 7

(OPTION)

Alterations in Erythrocyte and Hemostatic Function

Originally developed by:

Charlotte Lunse RN, MN

Revised (2000) by:

Karen Then RN, PhD

Associate Professor

Faculty of Nursing

University of Calgary

Unit 7 Table of Contents

Overview 4

Aim 4

Objectives 4

Resources 4

Web Links 4

Section 1: Anemia 5

Introduction 5

Clinical Manifestations 7

Etiology 7

Management 9

Learning Activity #1—Case Study 10

Section 2: Alterations in Coagulation 11

Introduction 11

Classification 13

Clinical Manifestations 13

Etiology 15

Evaluation and Treatment 17

Learning Activity #2 19

Learning Activity #3 20

Final Thoughts 21

References 22

Glossary 23

Acronym List 23

Checklist of Requirements 23

UNIT 7

Alterations in Erythrocyte and Hemostatic Function

In this unit, we will consider two main components of the hematologic system - erythrocytes and hemostasis factors. The third main component of the hematologic system are leukocytes. Function and alterations of leukocytes are discussed in the Immune System Unit.

In our approach to alterations in erythrocytes and hemostasis, we will focus on four components:

• alterations in erythrocyte production

• alterations in erythrocyte destruction/loss

• alterations in platelet function

• alterations in coagulation

Please note throughout this unit there are "fill in the blanks" sections. Work you way through these exercises as you do your readings. The answers are at the back of this unit.

Overview

Aim

The first aim of this unit is to increase your awareness and understanding of alterations in red blood cells, hemoglobin, platelets and hemostasis. The second aim is that you will gain an appreciation of your role in preventing, assessing and intervening in persons at risk for, or experiencing, anemia or coagulation disorders.

Objectives

1. Identify normal production and function of the erythrocyte.

2. Describe the pathophysiology and clinical manifestations of anemia.

3. Relate factors relevant to nurses for prevention, early identification and treatment of anemia.

4. Identify the normal pathway and process of hemostasis.

5. Describe the pathophysiology and clinical manifestations of coagulopathies.

6. Discuss factors relevant to nurses for prevention, early identification and treatment of alterations in hemostasis.

7. Discuss the potential impact of anemia or coagulation disorders on function of other body systems.

Resources

Requirements

• Porth, C. M. (2005). Pathophysiology – Concepts of Altered Health States (7th ed).

• Chapter 16. Red Blood Cell Disorders

• Chapter 15 . Disorders of Hemostasis

• Print Companion: Alterations in Erythrocyte and Hemostatic Function

Web Links

All web links in this unit can be accessed through the Web CT system.

Section 1: Anemia

Introduction

Although alterations of erythrocyte function usually include anemia and polycythemia, we will only focus our attention on anemia in this unit. Note it states in your text that neither anemia nor polycythemia are disease entities in themselves, but are described as “pathophysiologic manifestations of a variety of disease states”. This is a helpful perspective in some ways, but is also limiting in that anemia may result from a combination of factors, which do not necessarily include disease states. We will briefly consider common disease states, but will then focus on combinations of factors which result in a reduction of erythrocytes and/or hemoglobin.

Read the assigned review pages, or your preferred anatomy and physiology text and work through the exercise below.

Erythropoiesis is the production of erythrocytes, commonly referred to as red blood cells. The main physiologic regulator is erythroprotein, produced in the kidney and secreted in response to hypoxia. Erythropoietin production is also correlated with tissue metabolism and directly influenced by endocrine function, particularly pituitary and thyroid hormones.

Essential nutritional elements are required to produce normal erythrocytes, particularly vion, Vitamin B12 and folate (folic acid).

Erythropoiesis is also stimulated by testosterone (Rapaport, 1987), accounting in part for the normal differences in red blood cell count and hemoglobin levels between males and females.

Erythrocytes are uniquely designed and responsible for tissue oxygenation. The cytoplasm primarily contains hemoglobin (Hb), constructed of peptide chains and iron complexes (hemes). The iron in Hb is “red” when linked with oxygen (as is the oxidized iron in the roads in Avonlea, for any readers of Anne of Green Gables). Therefore iron gives not only erythrocytes but also blood its color.

Hemoglobin binds with a loose affinity with oxygen to provide transportation from the lungs to the tissues. In the lungs, almost 100 % of hemoglobin binds with oxygen.

At the tissues, approximately 25% of the oxygen is released. In addition to binding with oxygen, hemoglobin has an even greater affinity to carbon monoxide.

However, this binding is detrimental as CO is not easily released in either the lungs or tissues, and limits the oxygen carrying capacity of hemoglobin.

Not only are erythrocytes responsible for oxygen transport, they are also dependent on oxygen for normal function. Erythrocytes do not have mitochondria and require oxygen and glycolysis for energy to maintain cellular function and electrolyte balance. Oxygen is also required to meet the energy demands for preserving the shape and deformability of the red blood cell.

Clinical points

How would a decrease in deformability influence oxygen delivery at the tissue and organ level?

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Why may heavy smoking lead to a chronic decrease in the availability of hemoglobin for oxygen?

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Classification

InPorth (7th ed.)), anemias are classified broadly under two etiologic categories: decreased production and increased destruction. Anemias are also classified under three morphologic categories (reminder: morphology relates to structure and form). Structure and form within these categories of anemias refer to the erythrocyte’s shape and hemoglobin content.

Clinical Manifestations

Although your text describes clinical manifestations under each of the three morphologic categories, the manifestations are primarily similar, with specific differences in laboratory tests.

Persons with anemia may initially compensate for the low oxygen capacity. Symptoms of anemia may be subtle or only occur with an increase in oxygen demand, such as extensive exercise. Symptoms are diverse as many tissues and organs are affected and may include:

• fatigue

• weakness

• shortness of breath

• pallor

• change in appetite

• confusion

• infections

What would you see as a result of compensation by the heart and lungs?

Increase in:

• heart rate

• respiratory rate

• tidal volumes

Acute anemia, for example through hemorrhage, results in similar symptoms which are usually more readily perceived by the patient. However, note that blood loss may also occur over time and be covert, resulting in partial compensation and undefined symptoms.

Etiology

Recall persons you have seen through your professional career who had anemia (remember this includes decreased red blood cells and/or decreased hemoglobin).

What were the precipitating causes?

Let’s now consider the two main etiologic classifications of anemia, remembering that persons may have a combination of factors.

Alterations in Erythrocyte Production

Iron or vitamin deficiency may result in anemia “across the life-span”. In newborns, particularly premature babies or those with moms with an iron deficiency, iron stores may be depleted with the onset of erythropoiesis.

During puberty, both females and males are at risk for nutritional anemia due to increased demands with growth. A protein and/or vitamin deficient diet (i.e. intrinsic and Vitamin K) increases the adolescent’s vulnerability to nutrient deficiency anemia. Females are particularly vulnerable with the onset of menstruation and loss of hemoglobin.

As iron “recycling” is normally very efficient in the continual production of hemoglobin, a deficiency in iron intake alone is infrequently the primary cause of anemia. However, anemia may occur when one or more factors are combined with diet insufficiencies. Examples of other factors include: blood loss, chronic infection or alcoholism.

Alcoholics have several risk factors for anemia. Alcohol blocks the metabolism of folate (folic acid). In addition, the person with alcoholism may have a diet deficient in folate, iron and/or vitamin B12.

Infection, inflammation, malignancy and immune dysfunctions may result in a secondary anemia. Increased macrophage activity has been associated with decreased iron availability. Interleukin-1, released from macrophages, restricts iron availability; lactoferrin, released from neutrophils, binds with iron and the complex undergoes phagocytosis by the macrophages (Rapaport, 1987).

Alterations in Erythrocyte Destruction/Loss

Hemolysis or destruction of red blood cells (RBCs) may result in anemia. The causes of hemolysis may be intrinsic, such as infection, immune diseases, or hereditary defects in RBCs which result in their rapid removal. Extrinsic mechanisms include damage by antibodies, mechanical damage, infectious agents, medications and toxins.

As a cause of anemia, blood loss may be overt, covert, acute or chronic. An example of covert, chronic blood loss is menstruation. As you recall, women have a lower production of red blood cells due to lower levels of testosterone. In addition, Rapaport (1987) asserts that about 25% of menstruating North American women have no iron stores. This is attributed to a borderline deficiency in diet which minimally replaces menstrual loss. Potential for anemia in menstruation is exacerbated with irregular and extensive flow.

Management

Nursing interventions and medical treatment centre on first evaluating and then treating the cause of the anemia. Treatment is linked to the symptoms and tolerance of the person for the anemia. Lastly, factors required for erythropoiesis must be evaluated and optimized.

Nursing responsibilities include assessment for potential nutrition deficiencies, and teaching of nutritional requirements, which may occur in a variety of settings.

Iron absorption is primarily in the duodenum and upper jejunum. Vitamin C is necessary for iron absorption. Although iron is found in wheat and eggs, it forms insoluble complexes and is less readily absorbed. Iron from meat is readily absorbed as an intact heme molecule (Rapaport, 1987).

Folate (folic acid) is essential for DNA synthesis. It is found primarily in green vegetables, and also in fruit, beans, nuts, liver and kidney. A “tea and toast” diet may result in folate deficiency. Vitamin B12 is found in animal protein, including dairy products.

Assessment and prevention of blood loss require an attitude of suspicion and consideration of all possible sites of blood loss as well as potential hemolytic agents. Recall that RBCs may be destroyed by various medications or events. Also, recall that blood loss may be chronic and covert, such as gastrointestinal loss.

For acute and large losses of blood, a blood transfusion of packed red blood cells may be indicated. However the need for transfusion must be considered along with the following factors; the person’s need for blood, the availability of blood, risks with transfusion (such as blood borne viruses or reactions) and any personal or religious concerns.

Restoration of volume with oral or intramuscular iron replacements may also be considered, depending on the person’s risks due to anemia (Stowell, 1995). For example, a hemoglobin level of 70 mg/L may increase to 100 mg/L with 4 units of packed red blood cells. However, oral iron replacement will normally achieve this effect in 30 - 60 days (Stowell, 1995).

Learning Activity #1—Case Study

Rose, a 45 year old female, is driven to Emergency by her husband. She is pale, has rapid respiratory and heart rates. She is extremely fatigued and her story is supplemented by her husband at times. She indicates that she is having a change in menstruation and flow. She fainted in the shower and was unable to dress without assistance. She has been undergoing tests for a “low-thyroid”. When questioned, she agrees that she has been “a little tired”, especially when climbing a flight of stairs. You hypothesize that she is anemic

1. What factors and symptoms suggest anemia?

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8. What other information would be helpful to determine underlying pathophysiology in Rose’s anemia?

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9. You find out that Rose has been very busy at work and is concerned about her weight gain. She is skipping lunch and sometimes munching on breads and salads for supper. Rose’s Hb is 73 (normal: 120-140 g/l), her RBC is 4.2 (normal 4.7-6 106 /mm3).

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10. What nursing interventions would you initiate?

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11. What questions might you initiate with Rose or anticipate she may have?

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12. What medical treatment might you anticipate?

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Section 2: Alterations in Coagulation

Introduction

Platelets and clotting factors are required to maintain hemostasis. Hemostasis is a continual, complex and essential function, primarily orchestrated by platelets, clotting factors and lysis factors. Alterations in hemostasis result in decreased or inappropriate clot formation. We will explore alterations in platelets and alterations in coagulation.

Physiology Review

Hemostasis is ongoing in the microcirculation as shearing and minute injuries occur moment by moment. However, we tend to associate hemostasis with more extensive injuries. The purposes of hemostasis are to maintain blood volume, pressure and flow. Hemostasis also includes the dissolution or fibrinolysis of the clot, mediated by plasmin with fibrinogen and fibrin degradation products.

Two main events trigger formation of a blood clot: injury or platelet activation. Mediators which promote platelet activity are:

• collagen

• adenosine diphosphate

• platelet activating factor

The effects of platelet activation and the effect of platelets on clot formation are summarized on pages 287-89 in Porth.

Platelet aggregation is inhibited by the vascular endothelium and anticoagulants. Normally the endothelium prevents clotting through its smooth texture and negative charge.

Heparin is an endgenous anticoagulant, produced and secreted by mast cells and basophils. It has two main actions: halting the coagulation cascade and enhancing thrombin absorption.

Figure 7.1 illustrates the coagulation cascade and the intervention points for regular (unfractionated) heparin and low molecular weight heparin. Table 7.1 summarizes the respective clotting factors with their common names.

Figure 7.1 The coagulation cascade with sites of action of heparin (unfractionated heparin [UH] and low molecular weight heparin [LMWH].

Table 7.1 Blood Coagulation Factors

|Factors | |

|(international nomenclature) |Common Names |

|I |Fibrinogen |

|II |Prothrombin |

|IIa |Thrombin |

|III |Tissue Thromboplastin |

|IV |Calcium |

|V |Proaccelerin |

|(VI) |No longer considered distinct part of coagulation |

|VII |Prothrombin Conversion Accelerator, Proconvertin |

|VIII |Antihemophilic Factor |

|IX |Christmas Factor |

|X |Stuart Factor |

|Xa |Activated Stuart Factor |

|XI |Thromboplastin Antecedent |

|XII |Hageman Factor |

|XIII |Profibrinoligase, Fibrin Stabilizing Factor |

Then, K.L. & Rankin, J.A. (2000). Low molecular weight heparins (LMWHs): A review. Journal of Cardiovascular Nursing, 10(4), 37-41.

Classification

Alterations in hemostasis are often grouped into platelet disorders and coagulation disorders. Either disorder can cause inappropriate coagulation, resulting in bleeding or thrombus formation.

Disseminating intravascular coagulation (DIC) is not easily classified, as both clotting and hemorrage occur simultaneously.

Clinical Manifestations

Clinical manifestationss of altered hemostasis are not well described in your text, with the exception of DIC and altered hemostasis in children.

Bleeding or extensive bruising is the primary evidence of decreases in either platelet function or coagulation. An enlarged liver or spleen may be present.

Laboratory blood work includes platelet levels, prothrombin levels, partial thromboplastin time, and fibrinogen degradation products.

The normal platelet level is 150 - 300,000/mm3. Guidelines of risks with decreased platelet levels are indicated in the table below (Rapaport, 1987).

Table 7.2 Risks with decreased platelet levels

|Platelet number per mm3 |Risks |

|< 60,000 |tendencies for bleeding/bruising due to increased clotting time |

|< 20,000 |threat to central nervous system bleeding |

|< 5,000 |potential life threatening bleeding |

Prothrombin levels (PT) are used to evaluate extrinsic and common pathway factors; PT is particularly sensitive to vitamin K-dependent factors (Atkins, 1993). PT time has been replaced by “INR” to monitor vitamin-K dependent clotting factors and medications. INR - the International Normalized Ratio - is a more sensitive and consistent reference (Then & Rankin, 1999). Partial thromboplastin time (PTT) evaluates intrinsic and common pathway factors.

|Clinical point: |

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|Heparin primarily inhibits the instrinsic and common pathway of coagulation. |

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|Low molecular weight heparin inhibits Factor Xa from being produced. |

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|Warfarin (Coumadin) inhibits the production of Vitamin K-dependent coagulation factors in the liver. |

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|Based on the above description of PT/INR/PTT, indicate which test is used to monitor Heparin and Coumadin |

|therapy. Give rationale. |

Etiology

Alterations in platelet function may result from an increase or decrease in circulating platelets, or changes in platelet adhesion.

Changes in platelet adhesion are usually due a hereditary disease. For your interest, a protein called von Willebrand Factor (vWF) is also required for platelet adhesion. Absence of this factor (usually a hereditary condition) results in disorders in coagulation.

Thrombocytopenia (a decrease in circulating platelets) may result from:

• a decrease in number of platelets

• an increase in consumption or destruction of platelets

• an increase in sequesterian of platelets in the spleen

Disorders in coagulation relate to changes in availability of clotting factors.

The most common hereditary disorder is hemophilia.

Most frequently with hemophilia, there is a reduction in either factor VIII or IX (required in the intrinsic pathway). “Acquired” disorders of coagulation may result from Vitamin K deficiencies, liver disease or disseminated intravascular coagulation (DIC).

DIC is always a secondary complication from a precipitating event. The common outcome of these events is bleeding and thrombosis. Recall that normally fibrin clots are limited to formation at a vessel wall. In DIC, fibrin is formed in the bloodstream, and deposited in the microcirculation. The “excessive and inappropriate fibrin formation” (Dressler, 1993) depletes clotting factors (Figure 7.2). When clotting components are used in excess of their production, coagulation at sites of injury is inhibited. In addition, mechanical damage to RBCs from fibrin in the arterioles and capillaries results in hemolysis. Vascular occlusion, tissue necrosis, hemorrhage and shock occur.

If you would like further information on DIC, there are a list of optional readings listed in the reference section of this unit.

Alterations in the formation of thrombi may occur within arteries, veins, the heart or microcirculation of tissues or organs. Myocardial thrombosis is described in the unit on Alterations in Cardiovascular Function.

In venous thrombosis, the underlying mechanism differs. Vessel damage is not required, instead increased coagulability plays a key role. Stasis is important in development of venous thrombi as fibrin is allowed to form and thrombi extend over time. An increased propensity for developing thrombi may be hereditary or acquired. Additional factors associated with increased risk for thrombi are:

• surgery

• trauma

• increased age

• immobility

• artificial heart valves

• atrial fibrillation

• estrogen therapy

• pregnancy

• infection

• smoking

• obesity and

• stress

(Caswell, 1993)

[pic]

Figure 7.2 Consumption of platelets and clotting factors in the vascular system

Evaluation and Treatment

As with anemia, it is important to recognize and control bleeding in acute platelet or coagulation disorders . Transfusion of clotting factors has been the therapy of choice for hemophilia, unfortunately resulting in unforeseen medical, ethical and legal dilemmas due to blood-borne viruses, such as Hepatitis and HIV.

However, transfusion of blood products remains the treatment of choice for acute and severe blood loss. Replacement blood products include packed red blood cells, fresh-frozen plasma, cryoprecipitate, and platelets.

With active bleeding, Vitamin K is usually initiated until the underlying cause can be determined. Vitamin K:

• restores required nutrient levels in deficiency states

• facilitates production of clotting factors in liver disease

• increases the competitive availability with high coumadin (Warfarin) levels. Greater than therapeutic levels may occur with coumadin in relation to its long half-life and difficulty in developing the optimal dose

Learning Activity #2

1. Choose one of the precipitating mechanisms for DIC for which your client population is at risk.

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13. What nursing measures can you do to prevent or decrease the risk for DIC in this group?

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14. With this particular cause in mind, describe the treatment you would anticipate :

• removal of the underlying cause

• restoration of coagulation and fibrinolysis

• maintenance of organ function

The approach to thrombosis is primarily preventive through decreasing risk factors and the use of anticoagulants. Thrombi in the lungs, brain and heart are potentially life threatening.

Management is focused on early diagnosis and lysis of the thrombus to prevent disability or death. Acute and long term care of persons with venous thrombosis is controversial due to potential benefits and risks of anticoagulant therapy (Bick, 1995). Individual assessment and education are necessary to minimize or prevent risks.

Learning Activity #3

Alterations in hemostasis may be purposeful.

Investigate the underlying physiological mechanisms of medications influencing coagulation, such as:

• acetylsalicylic acid (ASA), warfarin (Coumadin)

• heparin, tissue-plasminogen activator (t-PA), low molecular weight heparin

Suggested references:

Catania, U. (1994). Monitoring coumadin therapy. RN, 57 (2), 29-34.

Hardman, J., Limbird, L., Molioff, Pl, Ruddon, R. & Goodman Gilman, A. (1996). Goodman and Gilman’s the pharmacological basis of therapeutics. New York: McGraw Hill.

Then, K.L. & Rankin, J.A. (1999). The International Normalized Ratio (INR): A review. Canadian Journal of Cardiovascular Nursing, 10 (1-2), 40-42.

Final Thoughts

In this unit we have explored aspects of the pathophysiology of the hematologic system. We primarily considered persons with anemia, platelet disorders and alterations in coagulation. These disorders and their underlying pathophysiology remain complex and are not yet well understood. Management requires thoughtful consideration of risks, benefits, assessment parameters and client education, particularly with blood transfusion and anticoagulant therapy.

References

Atkins, P. (1993). Postoperative coagulopathies. Critical Care Clinics of North America, 5(3), 459-473.

Bick, R. (1995). Oral anticoagulants in thromboembolic disease. Laboratory-Medicine 26(3), 188-193.

Caswell, C. (1993). Thromboembolic phenomena. Critical Care Clinics of North America, 5(3), 489-497.

Dressler, D. (1993). Patients with coagulopathies. In Critical Care Nursing, J. Clochesy, C. Breu, S. Cardin, E. Rudy, A. Whittaker (Ed). Toronto: W.B. Saunders.

Porth, C. M. (2005). Pathophysiology- Concepts of Altered Health states (7th ed). Philadelphia: Lippincott.

Then, K.L. & Rankin, J.A. (2000). Low molecular weight heparins (LMWHs): A review. Journal of Cardiovascular Nursing 10,(4) 37-41.

Then, K.L. & Rankin, J.A. (1999). The International Normalized Ratio (INR): A review. Canadian Journal of Cardiovascular Nursing, 10 (1-2), 40-42.

Stowell, C. (1995). When to pull the trigger. Laboratory-Medicine 26(1), 55-63.

The following articles are optional readings on DIC for your future reference:

Bell, T. (1993). Disseminated Intravascular coagulation: Clinical complexities of aberrant coagulation. Critical Care Nursing Clinics of North America. 5(3), 389-410.

Cate, H., Brandjes, D., Walter, Hl and van Deventer, S. (1993). Disseminated intravascular coagulation: Pathophysiology, diagnosis, and treatment. New Horizons, 1(2), 312-323.

Poole, J. (1993). HELLP syndrome and coagulopathies of pregnancy. Critical Care Nursing Clinics of North America, 5(3), 475-487.

Glossary

Acronym List

Checklist of Requirements

ڤ Print Companion: Alterations in Erythrocyte and Hemostatic Function

ڤ Porth, C. M. (7th ed).

■ Chapter 16. Red Blood cell Disorders

■ Chapter 15: Disorders of Hemostasis

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