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Bleeding Disorders

Also Known As: Coagulopathy

This article was last reviewed on October 10, 2012. This article was last modified on November 18, 2017.

What is a bleeding disorder?


A bleeding disorder is a tendency to bruise easily or bleed excessively or for prolonged periods. It may
be the result of certain genes that an individual has inherited or caused by conditions or factors that
develop within a person's lifetime (acquired).

Normally, blood remains in the circulatory system inside the blood vessels. When there is an injury to a
blood vessel or tissue and bleeding begins, the body stops the blood loss through a complex clotting
process called hemostasis. During primary hemostasis, the injured blood vessel constricts to reduce
blood flow and small cell fragments in the blood called platelets adhere to the injury site, clump together
(aggregate) with other platelets, and release chemical compounds that stimulate further aggregation of
other platelets to form a loose platelet plug. At the same time, activated platelets support the activation of
the coagulation cascade, a series of steps that involves the sequential activation of proteins in the blood
called clotting factors (coagulation factors). This secondary hemostasis process results in the formation
of strands of fibrin that weave through the loose platelet plug and compress to form a stable blood clot.
This barrier prevents additional blood loss and remains in place until the injured area has healed.

Hemostasis is a dynamic process, though, so once a clot is formed, certain factors are activated to slow
the clotting process. They eventually begin to dissolve the clot in a process called fibrinolysis so that the
clot is removed when the injury site is healed. In normal, healthy individuals, this balance between clot
formation and dissolution ensures that bleeding does not become excessive and that clots are removed
once they are no longer needed.

Each component of primary and secondary hemostasis must be present, activated at the right time, and
functioning properly for adequate clotting. If there are insufficient platelets or coagulation factors, or if
platelets or coagulation factors are not functioning normally, a stable clot may not form and a person
may be at an increased risk of excessive bleeding.

Bleeding disorders occur when something goes wrong with the clotting process, for example when a
component is missing, deficient, or not functioning properly. Disorders may involve problems with the
structure of the blood vessels, the production or function of platelets or one or more of the coagulation
factors, and/or the integrity and stability of the blood clot. Inherited bleeding disorders are rare and tend
to be caused by a deficiency or dysfunction of a single coagulation factor or clotting component.
Acquired bleeding disorders, those with no genetic component, are varied and occur more frequently
than inherited disorders.

Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. In
fibrinolysis, a fibrin clot, the product of the coagulation cascade, is broken down by a factor called
plasmin. Normally, an activator (which converts inactive plasminogen to active plasmin) is released into
the blood very slowly by the damaged lining (endothelium) of the blood vessels, such that, after several
days (when the bleeding has stopped and injury healed), the clot is broken down.

The fibrinolytic process is tightly regulated by several other factors, especially plasminogen activator
inhibitor (PAI) and plasmin inhibitor (e.g., alpha2-antiplasmin). If there is an inherited or acquired
deficiency in one of the inhibitors, the fibrinolytic activity is enhanced. As a result, the clot is not as stable
as it should be and is broken down early, causing excessive or prolonged bleeding, which typically
occurs after an injury or invasive procedure (e.g., tooth extraction, surgery).

About Bleeding Disorders

Structural Disorders

Excessive bleeding and bruising may be the result of blood vessels that have not formed properly
or do not function as they should. The following are a few examples:

Inherited

Hemorrhagic Telangiectasia – blood vessels are more fragile than usual, leading to recurrent
bleeding episodes; this rare disease affects approximately 1 in 50,000 people.
Ehlers-Danlos syndrome – collagen that supports blood vessels is unusually weak and elastic,
making blood vessels less protected and more prone to injury; this disease affects 1 in 10,000 to
20,000 live births.

Acquired

Allergic purpura – small blood vessels are inflamed and prone to leakage, a condition thought to
be an autoimmune response, and may be acute or chronic
Infectious purpura – blood vessels may be damaged directly by microorganisms or by toxin
produced by them; examples of causes include infections with Streptococcus or Staphylococcus
bacteria, Rocky Mountain Spotted Fever, and malaria.
Metabolic purpura – caused by a defect in metabolism; one example is vitamin C deficiency, also
called scurvy. This condition results in small blood vessels that have weakened walls due to a
defect in collagen synthesis. It is much less common now than it was a few hundred years ago
but can still be seen in areas of extreme poverty or war.
Platelet Disorders

Bleeding disorders may arise from problems with platelets, either from a low count in the blood or
from dysfunctional platelets. A CBC, which includes a platelet count, may reveal a low number while
platelet function tests may indicate that dysfunctional platelets are present. Several follow-up tests
may be required to determine the cause.

Platelet deficiency (thrombocytopenia)

A number of conditions and factors can cause a low platelet count, also called thrombocytopenia.
The causes typically fall into one of two general categories:

Disorders in which the bone marrow cannot produce enough platelets


Conditions in which platelets are used up (consumed) or destroyed faster than normal

Examples of conditions that can cause a low platelet count include:

Idiopathic (immune) thrombocytopenia, also called idiopathic thrombocytopenic purpura (ITP), is


caused by an autoantibody produced against platelets. It is one of the most common causes of
low platelets. Acute ITP occurs more often in youth, is usually short-term, and typically follows a
viral infection. This condition may resolve without treatment. Chronic ITP develops more slowly,
typically lasts longer than 6 months, and occurs more often in adults. Because of the duration of
the disease, this form may require treatment.
Heparin-induced thrombocytopenia (HIT) results in low platelets when a person who is on or
received heparin therapy develops an antibody. However, HIT is often associated with clotting,
rather than bleeding. (For more on this, see the article on HIT Antibody).
Thrombotic thrombocytopenia purpura (TTP) is an acute, potentially life-threatening though rare
condition. It causes both clotting and bleeding. Tiny clots form and deposit in small blood vessels
throughout the body. This clotting uses up platelets at an accelerated rate, leading to a low
number of platelets and increased risk of bleeding.
Certain drugs such as acetaminophen, quinine, sulfa antibiotics, digoxin, vancomycin, valium,
nitroglycerine and gold salts are just a few examples that have been associated with a decrease
in the number of platelets.
Disease-related:
Sepsis, especially that caused by a serious bacterial infection with Gram-negative bacteria
Cirrhosis
Autoimmune disorders, such as lupus, where the body's immune system produces antibodies
that attack its own organs or tissues, causing increased destruction of platelets
Cancer such as leukemia, lymphoma or another type that has spread to the bone marrow may
affect the production of platelets by the bone marrow. As the number of cancer cells increases
in the bone marrow, normal bone marrow cells are crowded out, resulting in fewer platelet-
producing cells.
Viral infections such as mononucleosis, hepatitis, HIV or measles
Aplastic anemia – with this condition, the production of all blood cells is significantly affected.
Massive blood (red blood cells) transfusion without giving platelets (thrombocytopenia due to
dilution effect)
Long-term bleeding problems (e.g., chronic bleeding from stomach ulcers)
Chemotherapy or radiation therapy, which may affect the bone marrow
Platelet consumption may be observed in various diseases and conditions. For example,
disseminated intravascular coagulation (DIC) and hemolytic uremic syndrome (HUS) can result
in fewer circulating platelets in the blood.
Increased pooling (sequestration) of platelets in enlarged spleen (e.g., related to cirrhosis,
myeloproliferative neoplasms)

Platelet dysfunction

The conditions and factors resulting in platelet dysfunction are either inherited or the result of some
other disease or condition (acquired).

Examples of inherited platelet function disorders include:

Glanzmann's thrombasthenia – affects platelets' ability to clump (aggregate)


Bernard-Soulier syndrome – characterized by reduced platelet adhesion
Storage pool disease – can affect platelet ability to release substances that promote aggregation

Acquired platelet dysfunction – those that are not inherited – may be due to chronic conditions or
factors such as:

Kidney failure (uremia)


Myelodysplastic syndrome (MDS)
Cardiopulmonary bypass surgery
Medications (e.g., aspirin and other nonsteroidal anti-inflammatory drugs)

Coagulation Factor Deficiency or Dysfunction

A bleeding disorder may be due to a lack of one or more clotting factors or the result of factors that
do not function properly. Deficiency or dysfunction of coagulation factors may have genetic causes
(inherited) or may be the result of another disease or condition. The following are a few examples:

Inherited

Von Willebrand disease (VWD): this condition is associated with decreased production or
dysfunction of von Willebrand factor and results in reduced platelet adherence to the injured blood
vessel and increased blood loss. VWD is the most common inherited bleeding disorder, affecting as
many as 1 in 100 people. Rarely, VWD may be due to an acquired VWF deficiency, where there is
no family or personal bleeding history up to the point of presentation.

VWD is separated into different types and sub-types, including:


Type 1 – with this type of VWD, there is a decrease in the amount of VWF produced, but the
VWF functions normally. Levels of factor VIII are also typically low but may be normal. This is the
most common type of VWD, accounting for about 75% of cases. It tends to cause bruising and
mild to moderate bleeding, such as persistent nosebleeds, heavy menstrual periods, and
prolonged bleeding following childbirth, trauma, dental procedures, and surgeries. Symptoms
and the severity of bleeding will vary from person to person and from episode to episode.
Type 2 – this type is typically associated with a normal amount of VWF, but the VWF does not
function normally. Bleeding may be more severe with this with this type. There are four different
subtypes, each caused by unique defects in VWF. Type 2 VWD accounts for 15-20% of all VWD
cases.
Type 3 – this rare type is associated with little to undetectable VWF production, very low factor
VIII levels, and moderate to severe bleeding. It is often detected in infancy because of early
bleeding episodes.

Hemophilia A (Factor VIII deficiency): This is an X-chromosome linked recessive bleeding disorder
that occurs primarily in males. It is the second most common inherited bleeding disorder, occurring
in 1 case per 5,000 males world wide. (For more on inheritance, see The Universe of Genetic
Testing.)

In those with the disease, the first bleeding episode may be with circumcision or other procedures
performed on an infant. The severity of the bleeding caused by a factor VIII deficiency depends on
its activity level. If it is very low, it may cause severe life-threatening bleeding; if it is moderate, it
may only cause mild to moderate bleeding, becoming an issue primarily when having surgery or
dental procedures.

Other inherited factor deficiencies include II, V, VII, X, XI, and IX (Hemophilia B, also called
Christmas disease, which is also X-linked and occurs in approximately 1 in 25,000 live male births).

Acquired

Liver dysfunction or disease – almost all coagulation factors are produced in the liver; liver
disease may result in decreased production of factors.
Vitamin K deficiency – the synthesis of several coagulation factors (II, VII, IX, X) requires vitamin
K.
Fat malabsorption
Exposure to snake venom
Some cancers
Treatment for cancer, such as chemotherapy or radiation therapy
Massive blood transfusions (e.g., transfuse only red blood cell units)
Factor inhibitors are antibodies that target a specific clotting factor, such as factor VIII,
decreasing its activity.
Anticoagulant drugs such as warfarin (COUMADIN®) or heparin; these drugs are used to treat
clotting disorders but in excessive amounts may cause bleeding.
Some bacterial infections
Disseminated intravascular coagulation (DIC), may cause both bleeding and clotting. It is usually
an acute condition, may be from a complicated childbirth, from an endotoxin produced during a
severe infection, or due to certain cancers such as a certain type of leukemia. DIC causes tiny
clot formation throughout the body, using up clotting factors at an accelerated rate, leading to
excessive bleeding.

Signs and Symptoms

Bleeding disorders may cause a wide range of signs and symptoms, depending on the cause.
Several different combinations of signs and symptoms may be present with varying degrees of
severity that changes over time. Bleeding may be severe, with episodes beginning in early
childhood, or relatively mild, involving prolonged bleeding following surgery, dental procedures, or
trauma.

Some signs and symptoms may include:

Unexplained or easy bruising


Frequent nosebleeds
Bleeding gums
Prolonged bleeding from small cuts or after dental procedures
In women, heavy menstrual periods that last longer than average
Joint and/or muscle pain or swelling after minor accident or injury
Small (<2 mm) red spots on the skin (petechiae); may sometimes look like a rash
Small (2-10 mm) purplish spots on the skin (purpura) or large (>10 mm) purplish lesions
(ecchymosis) caused by bleeding under the skin
Gastrointestinal bleeding, blood in the stool
Arthritic-type symptoms from damage from bleeding into joints
Loss of vision with bleeding in the eyes
Chronic anemia (often iron deficiency anemia)
When bleeding episodes begin early in life and/or when a close relative has an inherited factor
deficiency, an inherited bleeding disorder may be suspected.

Tests

If a doctor suspects that a person's signs and symptoms are due to a bleeding disorder, she may
order several laboratory tests. The investigation of a bleeding disorder is usually a step-by-step
process. A doctor may begin by ordering screening tests such as Prothrombin Time (PT) and Partial
Thromboplastin Time (PTT), which evaluate various components of the clotting process
(hemostasis), and a CBC to evaluate the number of platelets present and to determine if bleeding
has led to anemia. If the PT and/or the PTT are prolonged, for example, further testing may be done
to identify problems with coagulation factors and to see whether or not there may be factor specific
inhibitor.
The following table summarizes some of the tests that may be done in the investigation of a
bleeding disorder. Not all of the tests listed in the table are needed for each person with a
suspected bleeding disorder. The tests are listed in alphabetical order; for detailed information
about each test, click on the name of the test to go to the specific article.

Tests for Bleeding Disorders

The tests listed here are some of the more common tests performed to evaluate bleeding
disorders.

REASON FOR POSSIBLE SIGNIFICANCE


TEST DESCRIPTION
TESTING OF ABNORMAL RESULTS

Microscopic
examination of
blood; estimates
If platelet count Abnormal platelets may
Blood Smear the number and
is abnormal indicate a platelet disorder
evaluates
appearance and
size of platelets

Counts the
different types of
blood cells,
including
Routine screen
platelets, red Decreased platelets may
and general test
CBC (Complete blood cells indicate a platelet disorder;
to check for any
Blood Count) (RBCs), and anemia may indicate
abnormalities;
white blood cells excessive bleeding
detects anemia
(WBCs), types of
WBCs; measures
hemoglobin and
hematocrit

Individual tests to
measure the Decreased activity of one or
If PT or PTT
Coagulation Factors, activity (function) more factors may indicate
results are
Activity of specific factor deficiency or specific
abnormal
coagulation factor inhibitor
factors
REASON FOR POSSIBLE SIGNIFICANCE
TEST DESCRIPTION
TESTING OF ABNORMAL RESULTS

When the activity Low level may indicate factor


Measures the
Coagulation Factors, of a specific deficiency due to decreased
amount of
Antigen factor is production or increased
individual factors
consistently low consumption of a factor

If elevated, indicates recent


Measures a Evaluate blood clotting activity; may be due to
specific type of clot formation acute or chronic condition,
D-dimer cross-linked fibrin during bleeding such as a
degradation and clotting thrombosis, thromboembolism
product episodes or disseminated intravascular
coagulation (DIC)

Detects
antibodies
If coagulation If present, may cause specific
directed against
Factor Inhibitors factor activity factor deficiencies and
individual
test is abnormal excessive bleeding
coagulation
factors

If low, may indicate decreased


Reflection of Evaluate production or increased use;
Fibrinogen (activity) clotting ability and bleeding and may be elevated with infection
activity clotting and inflammation. It is an
acute phase reactant.

A general screen
that evaluates
factors XII, XI, IX, Prolonged PTT suggests
VIII, X, V, II need for further tests; may
(prothrombin), indicate
Partial Investigate
and I (fibrinogen) coagulation factor deficiency,
Thromboplastin Time bleeding
as well as specific inhibitor (such as
(PTT)
prekallikrein (PK) Factor VIII antibody),
and high nonspecific inhibitor (such as
molecular weight Lupus anticoagulant)
kininogen
(HMWK)
REASON FOR POSSIBLE SIGNIFICANCE
TEST DESCRIPTION
TESTING OF ABNORMAL RESULTS

Evaluate Evaluate
If abnormal, may indicate
Platelet Function platelets' ability to bleeding,
presence of one of several
Tests (aggregation adhere and form especially when
disorders including von
study) clumps platelet count is
Willebrand's disease
(aggregate) normal

A general screen Prolonged PT may suggest


Investigate
that evaluates need for further tests; may
Prothrombin Time bleeding or
factors VII, X, V, indicate coagulation factor
(PT) thrombotic
II, and I deficiency or dysfunction, or
episode
(fibrinogen) specific factor inhibitor

If decreased, may indicate


Indirect measure
Evaluate low vWF activity and
of von Willebrand
Ristocetin Cofactor bleeding decreased ability for platelets
factor (vWF)
episodes to adhere to injuries; may be
activity/function
due to von Willebrand disease

Help evaluate If elevated, heparin may be


Thrombin
bleeding contaminating blood sample;
activates
episode; also elevated with presence
fibrinogen to fibrin
sometimes when of fibrin degredation products,
Thrombin Time (TT) stands; TT
PTT prolonged; with very low levels of
detects presence
when heparin fibrinogen, and with abnormal
of inhibitors to
contamination fibrinogen (e.g.,
this process
suspected dysfibrinogenemia)

When activity
(measured as
If low, may indicate platelet-
Risocetin
von Willebrand Factor Measures related acquired condition or
Cofactor) is low;
(vWF) Antigen amount of vWF von Willebrand disease,
evaluate
increased risk of bleeding
bleeding
episodes
REASON FOR POSSIBLE SIGNIFICANCE
TEST DESCRIPTION
TESTING OF ABNORMAL RESULTS

When there is
Global need to assess
Abnormal result(s) could be
assessment of the potential
due to quantitative or
clotting abilities, cause of
qualitative defect in platelets,
including the excessive or
Thromboelastography coagulation factors, and/or
functional status prolonged
(TEG) fibrinolytic factors. The results
of platelets, bleeding during
are useful in guiding patient's
coagulation and after major
management, particularly
cascade, and surgery (e.g.,
blood product transfusion.
fibrinolytic activity cardiopulmonary
bypass)

Basic metabolic panels may be ordered to assess the liver and kidney functions. Patients with liver
and/or kidney failure have increased risk of bleeding.

Treatment

Treatment for a bleeding disorder depends on the cause, whether it is an acquired or inherited
condition, as well as on the duration and severity of signs and symptoms. Typically, bleeding
disorders are identified, monitored, and controlled both to prevent excessive blood loss and to
prevent complications that may arise. The degree and frequency of treatment needed will depend
on the severity of the deficiency or condition, whether or not there is a stimulus for bleeding such as
surgery or trauma, and whether or not the condition progresses or worsens over time.

If a bleeding disorder is due to an acquired condition, it may improve or worsen as the underlying
condition is resolved or progresses. If, for instance, factor deficiencies are due to a lack of
Vitamin K, they may return to normal with vitamin supplementation. If they are due to liver
disease or to a cancer, they will likely follow the course of the disease.

If a bleeding disorder is due to the development of antibodies, such as antibodies to factors VIII
or IX or to platelets, factor replacements or platelets transfusions may need to be given.
Sometimes different therapeutic products may need to be administered, such as corticosteroids
or other immunosuppressive drugs, to reduce antibody levels.
Sometimes simply avoiding injury, limiting physical contact sports for instance, and setting up the
daily environment to avoid cuts, bruises, and trauma may be enough to minimize bleeding
episodes in those with mild conditions, and under most circumstances, in those with moderate
bleeding tendencies.
Someone with severe deficiencies, such as Hemophilia A (factor VIII) and/or someone who is
having an acute bleeding episode will need to have one or more of their coagulation factors
replaced. Factor VIII and a few other individual factors are available in a concentrated form.
Multiple factor deficiencies or sometimes single factor deficiency can also be treated with
transfusions of fresh frozen plasma or plasma concentrates that contain all of the coagulation
factors. These concentrates and replacements can be given during a bleeding episode and as a
preventative measure before necessary surgeries and dental procedures to control excessive
bleeding.
If the bleeding disorder is due to dysfunctional or deficient platelets, units of platelets may be
transfused. If the disorder is due to von Willebrand disease or a mild form of Hemophilia A, a
drug called desmopressin (DDAVP) may be given to improve clotting temporarily. It causes the
release of stored factor vWF and may temporarily raise levels high enough and long enough to
allow procedures to be performed without transfusions.
With an acute condition, such as DIC, immediate treatment may be crucial and complicated.
Since DIC involves both clotting and bleeding throughout the body, treatment may involve
platelet and clotting factor transfusions as well as heparin or other anticoagulant therapy.

Related Content
On This Site
Tests: PTT, CBC, Coagulation Factors, D-dimer, Fibrinogen, PT, Platelet Function Tests , Thrombin
Time, von Willebrand Factor, Heparin-induced Thrombocytopenia Antibody
Conditions: Excessive Clotting Disorders, Liver Disease, DIC, Vitamin K Deficiency
Articles: Blood Banking: Blood and Components

Elsewhere On The Web


American Society of Hematology: Bleeding Disorders
National Hemophilia Foundation: What is a Bleeding Disorder?
Hemophilia Federation of America
Canadian Hemophilia Society
Womenshealth.gov: Bleeding disorder factsheet
MedlinePlus Medical Encyclopedia: Bleeding disorders
Platelet Disorder Support Association: Low Platelet Disorders
MayoClinic.com: von Willebrand Disease
MayoClinic.com: Hemophilia

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Article Sources

NOTE: This article is based on research that utilizes the sources cited here as well as the collective
experience of the Lab Tests Online Editorial Review Board. This article is periodically reviewed by the
Editorial Board and may be updated as a result of the review. Any new sources cited will be added to the
list and distinguished from the original sources used.

Sources Used in Current Review


Harmening D. Clinical Hematology and Fundamentals of Hemostasis. Fifth Edition, F.A. Davis Company,
Philadelphia, 2009, Pp 579-602, 611-630.

Wintrobe's Clinical Hematology. 12th ed. Greer J, Foerster J, Rodgers G, Paraskevas F, Glader B, Arber
D, Means R, eds. Philadelphia, PA: Lippincott Williams & Wilkins: 2009, Pp 1293-1300, 1335-1343,
1379-1383, 1388, 1394-1392.

(July 12, 2012) Zaiden, R., Hemophilia A. Medscape Reference article. Available online at
http://emedicine.medscape.com/article/779322-overview#a0156 through
http://emedicine.medscape.com. Accessed August 2012.

(April 6, 2012) Pollack, E., Von Willebrand Disease. Medscape Reference article. Available online at
http://emedicine.medscape.com/article/206996-overview through http://emedicine.medscape.com.
Accessed August 2012.

(August 1, 2010) National Heart, Lung and Blood Institute. What is thrombocytopenia? Available online
at http://www.nhlbi.nih.gov/health/health-topics/topics/thcp/ through http://www.nhlbi.nih.gov. Accessed
August 2012.

(March 14, 2012) National Heart, Lung and Blood Institute. What is Immune Thrombocytopenic Purpura?
Available online at http://www.nhlbi.nih.gov/health/health-topics/topics/itp/ through
http://www.nhlbi.nih.gov. Accessed August 2012.

(July 1, 2011) National Heart, Lung and Blood Institute. What is Hemophilia? Available online at
http://www.nhlbi.nih.gov/health/health-topics/topics/hemophilia/ through http://www.nhlbi.nih.gov.
Accessed August 2012.

Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL eds (2005). Harrison's Principles
of Internal Medicine, 16th Edition, McGraw Hill, Pp 673-680.

Henry's Clinical Diagnosis and Management by Laboratory Methods. 21st ed. McPherson R, Pincus M,
eds. Philadelphia, PA: Saunders Elsevier: 2007, Pp 735-743, 754-765.

American Society of Hematology. Bleeding Disorders. Available online at


http://www.hematology.org/Patients/Blood-Disorders/5219.aspx through http://www.hematology.org.
Accessed August 2012.

(June 1, 2011) National Heart, Lung and Blood Institute. What is Von Willebrand Disease? Available
online at http://www.nhlbi.nih.gov/health/dci/Diseases/vWD/vWD_WhatIs.html through
http://www.nhlbi.nih.gov. Accessed August 2012.

(May 22, 2012) Centers for Disease Control and Prevention. Hemophilia: What Should You Know?
Available online at http://www.cdc.gov/ncbddd/hemophilia/index.html through http://www.cdc.gov.
Accessed August 2012.

Sources Used in Previous Reviews


Thomas, Clayton L., Editor (1997). Taber's Cyclopedic Medical Dictionary. F.A. Davis Company,
Philadelphia, PA [18th Edition].

Pagana, Kathleen D. & Pagana, Timothy J. (2001). Mosby's Diagnostic and Laboratory Test Reference
5th Edition: Mosby, Inc., Saint Louis, MO.

Coagulation Test Panels. Clinical and Research Laboratories, Florida Hospital Cancer Institute [On-line
information]. Available online at http://www.fhci-
labs.com/researchlabs/clinicallabs/hemostasisandthrombosis/panels.htm through http://www.fhci-
labs.com.

Ryan, D. (2003 January). Platelet Function Testing. Strong Health Clinical Laboratories Newsletter, Vol.
28, No. 1 [On-line newsletter]. Available online at http://www.urmc.rochester.edu/path/newsletter103.htm
through http://www.urmc.rochester.edu.

Laposata, M. & Vancott, E. (2000 January). How to work up hypercoagulability. CAP In the News [On-
line Coagulation Case Study]. Available online at http://www.cap.org/CAPToday/casestudy/coag5.html
through http://www.cap.org.

Bleeding Disorders. The Merck Manual of Medical Information-Home Edition, Section 14. Blood
Disorders, Chapter 155 [On-line information]. Available online at
http://www.merck.com/mrkshared/mmanual_home/sec14/155.jsp through http://www.merck.com.

Venomous Bites and Stings. The Merck Manual of Medical Information-Home Edition, Section 24.
Accidents and Injuries, Chapter 287 [On-line information]. Available online at
http://www.merck.com/mrkshared/mmanual_home/sec24/287.jsp through http://www.merck.com.

Lee, D. (2000 July 24). Platelet Aggregometry. Stanford Interventional Cardiology [On-line information].
Available online at http://cvmed.stanford.edu/interventional/aggregometry.htm through
http://cvmed.stanford.edu.

Cortese Hassett, A. (2002). Platelet Function Testing. Transfusion Medicine Update, The Institute for
Transfusion Medicine, Issue #5 [On-line information]. Available online at
http://www.itxm.org/TMU2002/Issue5.htm through http://www.itxm.org.

Menta, S. (1999 Spring). The Coagulation Cascade. Physiology Disorders Evaluation, College of
Medicine, Univ of Florida [On-line information]. Available online at
http://www.medinfo.ufl.edu/year2/coag/title.html through http://www.medinfo.ufl.edu.

Elstrom, R. (2001 November 10, Updated). Factor X assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003680.htm.

Elstrom, R. (2001 November 10, Updated). Factor II assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003674.htm.
Elstrom, R. (2001 November 10, Updated). Factor II deficiency. MEDLINEplus Health Information,
Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000549.htm.

Elstrom, R. (2001 November 10, Updated). Factor IX assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003679.htm.

Elstrom, R. (2001 October 6, Updated). Hemophilia B. MEDLINEplus Health Information, Medical


Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000539.htm.

Elstrom, R. (2001 November 10, Updated). Factor V assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003675.htm.

Elstrom, R. (2002 May 6, Updated). Factor V deficiency. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000550.htm.

Elstrom, R. (2001 October 28, Updated). Platelet aggregation test. MEDLINEplus Health Information,
Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003669.htm.

Elstrom, R. (2001 November 25, Updated). Fibrinogen. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003650.htm.

Elstrom, R. (2001 November 13, Updated). Antithrombin III. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003661.htm.

Elstrom, R. (2001 October 28, Updated). Protein S. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003660.htm.

Elstrom, R. (2001 October 9, Updated). Factor VIII assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003678.htm.

Elstrom, R. (2001 October 14, Updated). Factor X deficiency. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000553.htm.

Elstrom, R. (2001 October 14, Updated). Factor XII (Hageman factor) deficiency. MEDLINEplus Health
Information, Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000545.htm.
Elstrom, R. (2001 November 10, Updated). Factor XII assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003681.htm.

Elstrom, R. (2001 November 25, Updated). PT. MEDLINEplus Health Information, Medical Encyclopedia
[On-line information]. Available online at http://www.nlm.nih.gov/medlineplus/ency/article/003652.htm.

Elstrom, R. (2001 October 28, Updated). Protein C. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003659.htm.

Elstrom, R. (2001 November 25, Updated). PTT. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003653.htm.

Elstrom, R. (2001 November 3, Updated). Fibrin degradation products. MEDLINEplus Health


Information, Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003655.htm.

Elstrom, R. (2001 October 21, Updated). Bleeding disorders. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/001304.htm.

Elstrom, R. (2001 November 10, Updated). Factor VII assay. MEDLINEplus Health Information, Medical
Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/003676.htm.

Elstrom, R. (2001 October 14, Updated). Factor VII deficiency. MEDLINEplus Health Information,
Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000548.htm.

Matsui, W. (2002 May 5, Updated). Primary or secondary fibrinolysis. MEDLINEplus Health Information,
Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000577.htm.

Matsui, W. (2002 February 2, Updated). Congenital antithrombin III deficiency. MEDLINEplus Health
Information, Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000558.htm.

Kovacs, B. (2001 November 26, Updated). Systemic lupus erythematosus. MEDLINEplus Health
Information, Medical Encyclopedia [On-line information]. Available online at
http://www.nlm.nih.gov/medlineplus/ency/article/000435.htm.

What is a Bleeding Disorder? (History). National Hemophilia Foundation, Bleeding Disorders Info Center
[On-line information]. Available online at http://www.hemophilia.org/bdi/bdi_history.htm through
http://www.hemophilia.org.
What is a Bleeding Disorder? National Hemophilia Foundation, Bleeding Disorders Info Center [On-line
information]. Available online at http://www.hemophilia.org/bdi/bdi_general.htm through
http://www.hemophilia.org.

Hemophilia A (Factor VIII Deficiency). National Hemophilia Foundation, Bleeding Disorders Info Center
[On-line information]. Available online at http://www.hemophilia.org/bdi/bdi_types1.htm through
http://www.hemophilia.org.

Bauer, K. (2001). The Thrombophilias: Well-Defined Risk Factors with Uncertain Therapeutic
Implications [20 paragraphs]. Ann Intern Med. 2001;135:367-373 [Journal]. Available online through
http://www.annals.org.

DeLoughery, T. (1999 March 15). Tests of Hemostasis and Thrombosis. OHSU [Online student handout].
Available online at http://www.ohsu.edu/som-hemonc/handouts/deloughery/printtest.html through
http://www.ohsu.edu.

McPherson R, Pincus M, eds, (2007). Henry's Clinical Diagnosis and Management by Laboratory
Methods, 21st edition, Saunders Elsevier.

© 2001-2018 by American Association for Clinical Chemistry

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