Download Section 1: Anemia - University of Calgary

Unit 7 Alterations in Erythrocyte and Hemostatic Function
UNIT 7
1
(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 .................................................................................................... 8
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
3
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.
4
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
5
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.
6
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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?
Why may heavy smoking lead to a chronic decrease in the availability
of hemoglobin for oxygen?
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.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
7
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
8
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
9
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).
10
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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?
2. What other information would be helpful to determine
underlying pathophysiology in Rose’s anemia?
3. 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).
4. What nursing interventions would you initiate?
5. What questions might you initiate with Rose or anticipate she
may have?
6. What medical treatment might you anticipate?
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
11
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.
12
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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].
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
13
Table 7.1 Blood Coagulation Factors
Factors
(international
nomenclature)
I
II
IIa
III
IV
V
(VI)
VII
VIII
IX
X
Xa
XI
XII
XIII
Common Names
Fibrinogen
Prothrombin
Thrombin
Tissue Thromboplastin
Calcium
Proaccelerin
No longer considered distinct part
of coagulation
Prothrombin Conversion
Accelerator, Proconvertin
Antihemophilic Factor
Christmas Factor
Stuart Factor
Activated Stuart Factor
Thromboplastin Antecedent
Hageman Factor
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.
14
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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
threat to central nervous system bleeding
potential life threatening bleeding
< 20,000
< 5,000
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:
Heparin primarily inhibits the instrinsic and common pathway of
coagulation.
Low molecular weight heparin inhibits Factor Xa from being produced.
Warfarin (Coumadin) inhibits the production of Vitamin K-dependent
coagulation factors in the liver.
Based on the above description of PT/INR/PTT, indicate which test is
used to monitor Heparin and Coumadin therapy. Give rationale.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
15
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
16
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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)
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
17
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.
18
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
19
Learning Activity #2
1. Choose one of the precipitating mechanisms for DIC for which
your client population is at risk.
2. What nursing measures can you do to prevent or decrease the
risk for DIC in this group?
3. 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.
20
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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), 2934.
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 (12), 40-42.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
21
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.
22
Unit 7 Alterations in Erythrocyte and Hemostatic Function
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 (12), 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.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 7 Alterations in Erythrocyte and Hemostatic Function
23
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