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SP16- Gen Path Exam 2 > Hemostasis and Coagulation > Flashcards

Hemostasis and Coagulation Flashcards

1
Q

What is hemostasis?

A

the ability to maintain blood in a fluid state (bleeding/clotting) and prevent loss from sites of vascular damage

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2
Q

What are the three major components of the hemostatic system?

A
  1. vascular wall
  2. platelets
  3. coagulation proteins
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3
Q

_______ results in platelet activation.

A

vascular injury that exposes subendothelial collagen

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4
Q

The hemostatic balance consists of opposing actions of ______ and _______.

A

procoagulant proteins

regulatory proteins

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5
Q

What are the three phases of Primary Hemostasis?

A

Adhesion
Activation
Aggregation

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6
Q

Platelet adhesion involves activation of the surface membrane receptor ______, the adhesion protein _______, and the appropriate surface, which is _________.

A

receptor: glycoprotein Ib/ IX
protein: von Willebrand factor
surface: subendothelial collagen

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7
Q

What does vWF do?

A

mediates the adherence of platelets to the subendothelial collagen

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8
Q

As platelets are activated by binding to vWF, there is a release of second messenger molecules within the platelet that leads to ____(4 events)____.

A
  1. shape change from discoid to spherical
  2. secretion of cyctoplasmic ADP
  3. activation of the glycoprotein IIb/IIIa receptor
  4. contraction of the platelet (mediated through active fibers)
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9
Q

What occurs during the aggregation stage of primary hemostasis?

A
  • platelets interact with other platelets
  • cytoplasmic ADP is released into the local milieu causing activation of adjacent platelets
  • platelet to platelet binding (mediated through fibrinogen and the gpIIB/IIIa receptor)
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10
Q

______ formation occurs with Primary Hemostasis, _______ formation occurs with Secondary Hemostasis.

A

Platelet Plug

Fibrin Clot

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11
Q

Describe the actions of thrombin.

A

Thrombin is generated through an amplification reaction via proteins within the plasma. Thrombin then converts fibrinogen to fibrin….fibrin adds stability to the clot after fibrin monomers are covalently cross-linked.

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12
Q

Fibrin monomers are covalently cross-linked by _____.

A

Factor XIII

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13
Q

Describe the sequence of activations in the intrinsic pathway.

A

Factor Xii is activated by Kallikrein
Factor Xi is activated by Xiia
Factor iX is activated by Xia

(12–11–9)

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14
Q

The extrinsic pathway refers to the sequence of activation of ______ by ______.

A

Factor Vii

by Tissue Factor

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15
Q

True or False: Calcium is a key element to the coagulation cascade.

A

True

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16
Q

The “common pathway” involves activation of _____, followed by conversion of ______. and then conversion of ______.

A

X to Xa
Prothrombin to Thrombin
Fibrinogen to Fibrin

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17
Q

How is a fibrin clot formed?

A

fibrin monomers are generated by thrombin and polymerize to form a long strand; monomers then cross-link due to actions of Factor Xiii (thirteen)

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18
Q

What is Antithrombin III?

A

a molecule which is activated in the presence of heparin and forms a complex with thrombin…by forming a complex, it destroys the ability of thrombin to participate in generation of fibrin monomers

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19
Q

What are the actions of the Protein C System?

A

Activated Protein C (APC) and Protein S (cofactor) will regulate/inactivate the major cofactors (Factors Va and Viiia) of the coagulation cascade

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20
Q

Deficiencies of Protein C or Protein S will result in ________ states.

A

hypercoaguable

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21
Q

What is the Factor V Leiden Mutation?

A
  • resistance to enzymatic inactivation by the Protein C/S complex
  • promotes coagulation
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22
Q

What does plasmin do?

A

breaks down previously cross-linked fibrin monomers into fibrin degradation products (FDP) and thus provides a mechanism for breaking down a previously formed clot during wound healing

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23
Q

How is plasmin activated?

A

TPA (tissue plasminogen activator)

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24
Q

True or False: TPA can be used therapeutically in patients who have had recent MIs since activation of plasmin is limited to the site of the clot.

A

True

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25
Q

What does antithrombin inhibit?

A

serine proteases

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26
Q

What are four (five) common laboratory screening tests used to evaluate hemostasis?

A
  1. Prothrombin Time (PT)
  2. International Normalised Ratio (INR)
  3. Partial Thromboplastin Time (PTT)
  4. Platelet Count
    Bleeding Time (no longer used)
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27
Q

______ is a measurement of the time needed for plasma to form a clot in the presence of added tissue thromboplastin and calcium ions.

A

Prothrombin Time (PT)

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28
Q

Prolonged PT can result from decreases or abnormalities in Factors ________ and/or _______. These proteins are all important in which pathway?

A 
Vii
X
V
ii
fibrinogen

EXTRINSIC pathway

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29
Q

What is the International Normalised Ratio?

A

a ratio of the patient PT time compared to a “control-PT time” that allows for comparison between laboratories
*also used to monitor anticoagulant patients

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30
Q

_____ screens for activity within the INTRINSIC pathway which includes Factors ______ and fibrinogen.

A

Partial Thromboplastin Time (PTT)

(fibrinogen 10, 5, and 2 are in both! 7 is in extrinsic only)
Factors:
Xii
Xi
X
iX
Viii
V
ii
(12, 11, 10, 9, 8, 5, 2)
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31
Q

What does the “platelet count” measure?

A

a measurement of platelet number in ANTIcoagulated blood; quantified by an automated instrument

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32
Q

What is the normal range for platelet count?

A

150,000 to 400,000 microliters

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33
Q

What is thrombocytopenia?

A

a decrease in platelet NUMBER

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34
Q

What is thrombocytosis (or thrombocythemia)?

A

an increase in platelet number

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35
Q

Which laboratory test is used to measure the degree of anticoagulation in patients receiving oral anticoagulants such as coumadin/warfarin?

A

PT (prothrombin time-measures time to form a clot)

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36
Q

What does PTT (partial thromboplastin time) measure?

A

PTT measures the time needed for plasma to form a clot in the presence of added ground glass(Kaolin), cephalin, and calcium ions
*The glass activates “contact dependent” Factor Xii

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37
Q

PTT is routinely used to measure degree of anticoagulation in patients receiving _______ therapy.

A

Heparin

PTT measures intrinsic path and heparin
PT measures extrinsic path and warfarin/coumadin
(WEPT = warfarin, extrinsic, prothrombin time)

38
Q

What has “bleeding time” been replaced by?

A

PFA-100

-performs like an in vitro bleeding time

39
Q

If either the PT or PTT is prolonged, what is to be done?

A

a mixing study

  • using a 1:1 ratio of normal plasma to patient plasma
  • by mixing in 50% of a given factor, there should be a normalized PT or PTT
  • if the mixing study is corrective of clotting time = deficiency of some FACTOR exists
  • if the mixing study does not correct clotting time = an INHIBITOR is thought to be present (antibody)
40
Q

What are three specialized tests that may be performed after an un-corrected mixing study?

A
  • Factor Assays (for specific coagulation factors)
  • Circulating Anticoagulant (fibrinogen amount and fxn)
  • Platelet Aggregation Testing
41
Q

What is the difference between a Congenital bleeding disorder and an Acquired disorder?

A

Congenital: present at birth, usually
Acquired: occur after birth and are often related to mediation or other pathologic processes

42
Q

Bleeding that is primarily mucosal suggests a ______ problem; whereas, presence of deep tissue hematomas would suggest ________.

A

platelet

a defect in coagulation proteins

43
Q

What type of disorder is suspected if screening lab tests are normal?

A

disorders of the regulatory system

44
Q

What are the clinical manifestations of Primary Hemostasis Disorders? What are the lab findings?

A

Clinical:

  • mucocutaneous bleeding
  • excessive bleeding with trauma

Lab:

  • Prolonged bleeding time (PFA-100)
  • Thrombocytopenia
45
Q

What are the clinical manifestations of Secondary Hemostasis Disorders? What are the lab findings?

A

Clinical:

  • Soft tissue bleeding
  • Excessive bleeding with trauma

Lab:

  • Prolonged PT and PTT
  • Prolonged Thrombin Time (TT)
46
Q

What are the clinical manifestations associated with Disorders of the Regulatory System? What are the lab findings?

A

Clinical:

  • soft tissue bleeding
  • excessive bleeding with trauma

Lab:

  • normal PT and PTT
  • normal bleeding time
  • normal platelet counts
47
Q

What are the three mentioned Congenital Bleeding Disorders?

A
  1. von Willebrand Disease
  2. Factor VIII deficiency (hemophilia A)
  3. Factor IX deficiency (hemophilia B)
48
Q

______ functions as both a carrier molecule for Factor VIII and as the “glue” between damaged endothelium and platelets.

49
Q

Where is Factor VIII synthesized? Where is vWF located?

A 
VIII = in the liver
vWF = platelets and endothelial cells
50
Q

What is the Factor VIII Complex composed of?

A

vWF (large molecule composed of associated multimers)
+
Factor VIII Procoagulant

51
Q

von Willebrand Disease is an autosomal _____ disorder that is associated with production of _______ amounts of a normal protein OR production of a protein with abnormal function (quantitative, qualitative, both).

A

dominant
decreased

(most common form of this disease is decreased amounts of vWF)

52
Q

What is the dominant clinical manifestation of von Willebrand Disease?

A

mucocutaneous bleeding

nosebleeds, bruises, excess menstrual flow, etc

53
Q

True or False: von Willebrand Disease is the most common inherited bleeding disorder and occurs in approximately 1% of the US population.

54
Q

True or False: Symptoms of von Willebrand disease often get worse after adolescence.

A

False, often improve

55
Q

What are the three types of vWD?

A

Type 1: quantitative deficiency (partial)
Type 2: qualitative deficiency
Type 3: quantitative deficiency (total)- most severe

56
Q

What are the laboratory features of vWD?

A
  • decreased Factor VIII
  • decreased vWF
  • prolonged bleeding time (PFA-100)
  • prolonged PTT

(BEND: bleeding time prolonged, endothelium derived, normal to low platelets, desmopressin for treatment)

57
Q

________ releases vWF from endothelial cells and is the common drug for treating vWD. What is the most recent treatment option for vWD?

A

Desmopressin

Recombinant Factor VIII

58
Q

Hemophilia A is a(n) __________ disorder that occurs due to decreased production of Factor ____.

A

x-linked recessive

VIII

59
Q

True or False: Hemophilia A is the most common hereditary cause for serious bleeding.

60
Q

What is the clinical hallmark of Hemophilia A?

A
  • recurrent soft tissue bleeding

* symptoms usually start early in life*

61
Q

True or False: There is a high rate (30%) of spontaneous gene mutations responsible for the appearance of new vWD cases in non-carrier families.

A

False, that statement holds true for Hemophilia A

62
Q

What is hemarthrosis associated with?

A

Hemophilia A (unusual course of bleeding into joint spaces, causing fibrosis)

63
Q

Where does bleeding occur with Hemophilia A?

A 
Joint spaces (hemarthrosis)
soft tissues
intramuscular (hematomas)
intracerebral (hemorrhage)
64
Q

Which laboratory values are altered with Hemophilia A?

A 
PTT  (prolonged)
Factor VIII (decreased)

-the others are normal

65
Q

Complications of Hemophilia A (or B) include ________, _______, and _______.

A 
joint disease
pseudotumors
fatal hemorrhage (intracranial or retroperitoneal)
66
Q

_____-______ complications of hemophilia A include transfusion-transmitted diseases, formation of antibodies to transfused VIII, allergic reactions, and hemolysis.

A

therapy-related

67
Q

What type of disorder is hemophilia B? How does it differ from hemophilia A?

A

x-linked recessive disorder

B is less common and is associated with a decreased production of Factor IX (rather than Factor 8)

68
Q

What is thrombocytopenia?

A

a decrease in platelet count; generally, when the platelet count is less than 100,000 microliters
*spontaneous bleeding manifests when the count falls below 20,000

69
Q

How does bleeding due to thrombocytopenia typically appear? How else can thrombocytopenia be evaluated?

A

petechial hemorrhage in skin and mucous membranes

  • peripheral blood smear
  • bone marrow examination (megakaryocytes, etc)
  • platelet antibody determination
70
Q

By what mechanisms can thrombocytopenia develop?

A
  1. Decreased production of platelets
  2. Increased destruction of platelets (aplastic anemia)
  3. Sequestration (pulled out of circulation)
  4. Congenital or Acquired
71
Q

____ ____ _____ is a disorder characterized by immune-mediated destruction of platelets (autoantibodies directed at the platelet membrane antigens)

A

Immune Thrombocytopenic Purpura (ITP)

72
Q

Which platelet membrane antigens are commonly targeted in Immune Thrombocytopenic Purpura (ITP)?

A

Glycoprotein Ib/IX

Glycoprotein IIb/IIIa

73
Q

With ITP, increased IgG bound to the platelet surface promotes increased sequestration by the ________ system and _______.

A

reticuloendothelial

spleen

74
Q

Describe the two forms of ITP.

A

Acute: occurs in childhood, common viral prodrome, sudden onset, severe thrombocytopenia, frequent spontaneous remission, affects males and females equally

Chronic: gradual onset, occurs in adults, infrequent spontaneous remission, moderate thrombocytopenia, no viral/antecedent infection, more common in females

75
Q

What are the therapy options for ITP?

A
  • corticosteroids
  • IV immunoglobulin
  • splenectomy
  • immunosuppression
76
Q

Clinical Features of ITP include bleeding with trauma, _______ and ______.

A

petechial hemorrhages

ecchymoses (bruises)

77
Q

True or False: With ITP there are no microangiopathic changes on blood smear review.

A

True, no evidence of RBCs being sheared apart by thrombocytes

78
Q

________ is an acute disorder characterized by intravascular platelet activation with formation of platelet-rich microthrombi throughout the circulation.

A

Thrombotic Thrombocytopenic Purpura (TTP)

79
Q

TTP is now known to be caused by a deficiency of a metalloproteinase that normally degrades very-high molecular weight multimers of vWF. What is the name of this metalloproteinase?

80
Q

What does ADAMTS 13 do?

A

degrades very high molecular weight vWF

81
Q

True or False: Deficiency of ADAMTS 13 is an inherited disorder, not acquired.

A

False, TTP (enzyme deficiency) can be either inherited or acquired

82
Q

True or False: TTP can be left untreated without major repercussions.

A

False, high mortality rate if untreated

83
Q

Treatment of TTP involves _____ to replace the ADAMTS 13 enzyme.

A

plasmaporesis

84
Q

What are the clinical manifestations of TTP?

A 
fever
marked thrombocytopenia
microangiopathic hemolytic anemia
acute renal failure
neurologic changes (headache, mental status changes)
85
Q

What cell will appear in the peripheral blood smear of a TTP patient?

A

schistocytes

86
Q

In TTP, the increased ______ and ______ reflect intravascular hemolysis.

A

bilirubin
Lactate Dehydrogenase

(body is breaking down RBC too quickly)

87
Q

With DIC there is both systemic ______ formation and systemic ______ formation.

A

thrombin

plasmin

88
Q

What is DIC?

A

unregulated, widespread intravascular activation of the hemostatic system; coagulation factors are activated and consumed faster than they can be produced which results in bleeding and microthrombi; platelets are also consumed which results in thrombocytopenia

89
Q

What are four clinical situations with increased risk for occurence of DIC?

A
  1. Infections (gram negative sepsis)
  2. Tissue Injury (trauma, burn, surgery, venomous snake bites, vasculature lesions, etc.)
  3. Obstetrical Complications
  4. Certain Malignancies
90
Q

How is DIC managed/treated?

A

therapy aims to:

  1. remove or reverse the initiating stimulus,
  2. support the patient’s coagulation protein reserve
91
Q

How is the patient’s coagulation protein reserve “supported?”

A

-transfusions of blood products (plasma and platelets)

92
Q

What are the blood products that are used for transfusions in DIC patients?

A
  1. FFP (coagulation and regulatory proteins)
  2. Cryoprecipitates (fibrinogen, VIII, vWF)
  3. Platelets

SP16- Gen Path Exam 2 (7 decks)

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