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Pathology Exam 3 > Coagulation Lectures > Flashcards

Coagulation Lectures Flashcards

1
Q

What is hemostasis

A

A process where an injured blood vessel triggers a series of reactions

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2
Q

How does hemostasis work

A

Formation of platelet fibrin to plug injury site to stop blood loss.

Clot will dissolve gradually as healing advances

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3
Q

What are the components of Hemostasis

A

Coagulation factors

Platelets

Endothelium - vessel wall

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4
Q

What is the role of platelets in coagulation?

A

Adherence to injury site where collagen is exposed

platelets activate by thrombin.

Release ADP, Vasoactive amine and form Thromboxane A2

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5
Q

What does Thromboxane do?

A

Contracts Smooth Muscle - Causes vasoconstriction - stops blood leakage

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6
Q

What are the steps of clot formation

A

Procoagulant proteins are activated by proteolytic cleave to form a clot

Goal is to product thrombin

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7
Q

How does thrombin work?

A

Convers fibrinogen to fibrin - makes fibrous network in clot

Promotes platelet aggregation to seal injury as well

Also activates cofactors (V and VIII) and factors to lyse clot

Activates protein C to prevent uncontrolled thrombosis

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8
Q

Describe control of Coagulation

A

Clotting cascades and platelets are inhibits by vascular endothelium and continuous blood flow

Natural anticoagulant proteins

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9
Q

What are some of the anticoagulant proteins?

A

Anti-Thrombin III - binds to heparin and thrombin to inactivate

Protein C - cleaves factors V and VIII

Protein S - cofactor to protein C

Tissue Factor Pathway Inhibitor - Inhibits Xa and VIIa-TF complex

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10
Q

What are physiologic Anticagulants

A

Antithrombin III

Protein C and S

Tissue Factor Pathway Inhibitor

Thrombomodulin

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11
Q

Describe Fibrinolysis

A

Fibrin is degraded by plasmin

Plasminogen is activated by TPA

Fribinolysis is inhibited by plasminogen activator inhibitors (PAIs) and Alpha 2-Antiplasmin

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12
Q

Role of Vitamin K in Coagulation

A

All serine proteases require post translational mods which require Vitamin K

Need vitamin K and adequately functioning liver

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13
Q

What is the most widely used anticoagulant drug?

A

Warfarin (Coumadin) interferes with Vitamin K Dependent reactions

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14
Q

What does Prothrombin Time measure?

A

PT measures procoagulant activity of factors VII, X, V, II and fibrinogen.

PT normal range is 9-12 seconds.

Results compared to an International Normalized Ratio = 1.0 = normal

Long PT = Deficiency of Vit. K factors

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15
Q

What does Activated Partial Thromboplastin Tim (APTT/PTT) measure?

A

Measures the procoagulant activity of entire pathway

Most sensitive to XI, VII, and IX. not effected by VII

Can be prolonged also by drugs like heparin.

25-32 seconds

Hemophiliacs = prolonged

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16
Q

Thrombin Time (TT) measurement

A

Measures platelet and vessel interaction, # and function of platelets

Performed by making cut on forearm

Tim to clotting is measured

2-9 minutes. Severe platelet decrease will prolong bleeding time

prolonged by Von Willebrand disease

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17
Q

PFA-100

A

New - Platelet Function Analyzer

Tests in vitro bleeding time

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18
Q

What is Hemophilia A and B a deficiency of?

A

Factors VIII and IX

X-Linked

Females are carriers

Prolonged PTT

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19
Q

Describe Hemophilia A

A

Factor VIII deficiency - Most common cause of severe bleeding tendency

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20
Q

Describe Hemophilia B

A

Christmas disease or Factor IX deficiency

10 times less common than A

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21
Q

Severe Hemophilia

A

<1%
Spontaneous hemorrhaging

Early Death before factor replacement therapy.

Can lead to severe arthritis

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22
Q

Moderate Hemophilia

A

2-5%

Takes some degree of trauma to cause bleeding

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23
Q

Mild Hemophilia

A

10%

Only bleed after trauma

Need specific factor therapy to resolve bleeding

Can have hematoma formation, wound breakdown, disability if not treated during surgery

Dinged after bad traumatic event or surgery

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24
Q

Carrier Females

A

30%-100%

Carriers can be mildly affected or normal

Carriers w/bleeding - symptomatic carrier

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25
Q

Factor IX Deficiency

A

Congenital Disorder - autosomal recessive

Spontaneous bleeding is rare

Ashkenazi Jews in US and Middle East

Post-Operative Hemorrhage

Prolonged PTT

26
Q

Von Willebrand Disease

A

Most common congenital - Autosomal dominant

Large protein in plasma

Adheres platelets to collagen = prolonged bleeding time

Carries Factor VIII = decreased factor VIII prolongs PTT

Nose bleeds/Mucosal bleeds

27
Q

What are the two types of Von Willebrand disease?

A

Type 1 - Deficiency - Treat with DDAVP

Type 2 - Abnormal Protein
2b - Abnormal clearance of platelets

Type 3 - severe or total deficiency

28
Q

6 Tests for Von Willebrand Disease

A
  1. Bleeding Time - Platelet function
  2. vWF Antigen - Amount of factor
  3. VWF activity - function of factor to aggregate platelets
  4. Factor VIII activity - ability to carry VIII
  5. Multimeric Analysis - Loss of large forms
  6. RIPA - hyperaggrebility to ristocetin to diagnose type 2b
29
Q

Acquired bleeding disorders that cause prolonged PTT

A 
Herpain in sample
Hemophilia A and B
Factor XI Deficiency
Factor XII Deficiency - no bleeding
Acquired Hemophilia
Von Willebrand Disease
Lupus Anticoagulant - No bleeding
30
Q

Acquired bleeding disorders that cause prolonged Pro Time

A
  1. Protime more prolonged than PTT = liver disease, Vit. K Deficiency, Warfarin/Rat Posion
  2. PTT more prolonged = Disseminated Intravascular Coagulation (DIC)
31
Q

How does Liver Disease affect Coagulation?

A

Can cause deficiencies in clotting factors.

Severe liver disease = Low Fibrinogen = possible Thrombin prolonged

Prolonged Protime

Consumption of platelets by spleen

Deficiencies in antithomrbin III and Protein C/S

32
Q

How does Vitamin K Deficiency Affect Coagulation

A

Prolonged protime

Occurs when patients do not intake Vit. K through diet

Broad Spectrum Antibiotics can kill gut flora (makes Vit. K)

33
Q

How does Long Acting Fat Soluble Rat Points affect coagulation?

A

Used in suicide attempts

Extremely prolonged protime and PTT

Intensive Vit. K therapy for months is required

34
Q

Disseminated Intravascular Coagulation (DIC)

A

Can be caused byMassive Trauma, hemorrhagic, septic shock, amniotic fluid embolism, burns, acute leukemia

Micro thrombi plug capillaries and causes tissue infarction

Coagulation Factor deficiencies

Low levels of fibrinogen and platelets

Prolonged PTT due to fibrin split products

35
Q

Abnormalities in DIC (6)

A 
Prolonged PT
Greatly Prolonged PTT
Prolonged Thrombin Time
Low platelet count
Low fibrinogen level
Increased fibrin split products
36
Q

Define Thrombosis

A

Formation of clot within vasculature

Occurs with stasis, inflammation and vessel wall injury

37
Q

Virchow’s Triad

A
  1. Decreased blood flow (venous stasis)
  2. Inflammation of or near the injured Blood vessel
  3. Intrinsic alterations in nature of the blood
38
Q

When do arterial thrombi occur?

A

Conditions of shear stress

Composted of aggregated platelets (white thrombi)

39
Q

What abnormalities can contribute to Arterial thrombi development?

A

hypertension & turbulent blood flow @ arterial branch points and sites of atherosclerosis

40
Q

What blood vessel abnormalities contribute to Arterial thrombi (5)

A

intraluminal vascular endothelial cell injury

atherosclerotic plaque rupture

Hyperhomocysteinemia

Aneurysm foramtion

Vessel Dissection

41
Q

When does Venous Thrombi occur?

A

Slow blood flow (low shear stress)

Composted of large amounts of fibrin (red thrombi)

42
Q

What factors contribute to venous thrombi? (7)

A 
R. Side heart failure,
Pre existing thrombosis
Tumor compression
Immobility
Obesity
Chronic venous insufficiency
Increased Age
43
Q

What are some Symptoms of Venous Thromboembolic Disease?

A

50% Asymptomatic
Phlegmasia ceruleans dolens (swollen, blue, painful leg)
Pain
Pitting Edema
Warm,Dusky,Reddish-blue discoloration on skin

44
Q

Complications/Consequences of Extermity DVT

A

Postthombotic Syndrome - Chronic Swelling, cutaneous ulcers

Pulmonary Embolus - Infarct

45
Q

Classic Signs and Symptoms of PE (6)

A 
Chest Pain
Dyspnea
Anxiety
Cough
Syncope
Cyanosis
46
Q

Diagnosis of DCT and PE

A

D-Dimer Assay - only occurs in clots

Venous UltraSound - Measures blood flow/pressure 95% specificity to symptomatic DVT

Spiral CT for PE and V/Q scans

47
Q

Treat of Arterial Thrombosis

A

Acute: Heparin and Fibrinolytic agents (tPA)

Prevention: Antiplatelet agents: aspirin, thienopyridines, ticlopidine, clopidogrel

48
Q

Treatment of DVT and PE

A

Acute: Heparin - to activate antithrombin III

Long term:Oral Anticoagulation with Warfarin: doesn’t affect coagulation factors that are already released. Heparin therapy at least 5 days after starting

49
Q

How long is anticoagulation therapy generally

A

Individual basis: must determine if DVT occurred due to transient risk factors or underlying disorder

Location of clot influences

50
Q

Hypercoagulable States

A

Exist when:
chronic damage to vessel walls

Excess of procoagulant factors

deficiency of anticoagulant factors

51
Q

What are 4 clues to underlying Hypercoagulable state

A
  1. Thrombotic episode in absence of conditions
  2. Recurrent episodes of thrombosis
  3. Severe, life threatening thrombosis
  4. Family History
52
Q

What is Factor V Leiden Inherited Thrombotic Disorder?

A

Autosomal Dominant mutation of Factor V Gene

Inactivation through proteolytic cleavage of protein C

most common in northern european caucasian populations

53
Q

What is Prothrombin G20210A Gene Mutation Inherited Thrombotic Disorder?

A

Second most common

Elevated concentrations of plasma prothrombin

54
Q

What is Protein C Deficiency Inherited Thrombotic Disorder?

A

Autosomal Dominant

Heterozygotes more effected

31 fold increased risk

Large Doses of Warfarin increase risk

55
Q

What is Protein S Deficiency Inherited Thrombotic Disorder?

A

Autosomal Dominant

Pts. present with VTE or Arterial Thrombosis including stroke

56
Q

Antithrombin Deficiency

A

Autosomal Dominant

Homozygous fatal in utero

40 fold thrombosis risk

Can lead to heparin resistance

57
Q

Hyperhomocyteinemia

A

Inherited or acquired

Increased risk of thrombosis enhanced platelet activation due to endothelial cell injury

58
Q

Increased Factor VIII Activity (>150%)

A

3-6 fold greater risk of VTE

11 fold @ >200%

59
Q

Impaired Fibrinolysis

A

Plasminogen Deficiency, tPA deficiency

Increased thrombosis risk

60
Q

Oral Contraceptives

A

Increased thrombosis risk by altering coagulation factor levels

61
Q

The Lupus Anticoagulant

A

Common Acquired Abnormality - Hypercoaguable State

IgG Antibody

Antiphopholipid Antibody Syndrome (APL)

Prolongs PTT

No bleeding tendency

Thrombotic Syndrome

Pathology Exam 3 (4 decks)

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