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Clin Med- Heme/Oncol > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What does the healing process consist of?

A 
Blood Clotting
Inflammation & the Immune Response
Wound Healing
Termination of Blood Clotting
Clot Lysis
Termination of Inflammatory Response, the Immune Response and Wound Healing
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2
Q

What are 4 clotting factors?

A

Platelets
Soluble Clotting Factors
Tissue Factor
Collagen & Phospholipids

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3
Q

What are 5 anti clotting factors?

A 
Nitric oxide (NO)
Protein C & S
Anti-Thrombin III
Fibrinolytics
Prostacyclin
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4
Q

What are 3 vessel bound clot inhibitors?

A

Vascular Endothelial ADPase
Prostacyclin
NO

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5
Q

What are 4 vessel bound clot initiators?

A

Tissue Factor
von Willebrand Factor
Collagen
Thromboxane A2

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6
Q

2 tests of clotting ability

A

protime (PT)

Activated Partial Thromboplastin Time (aPTT)

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7
Q

Protime (PT)

A

Most Sensitively Measures the Concentration of Clotting Factors in the Extrinsic Pathway and the Common Pathway, Many of Which Depend on Vitamin K for their Activity: F II, F VII, F IX, & F X

PT is prolonged when coumadin decreases the vit K factors

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8
Q

aPTT

A

Most Sensitive to the Concentration of Clotting Factors in the Intrinsic Pathway and the Common Pathways: F XI, F IX, F VIII, F X, F II (Prothrombin) & Fibrinogen

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9
Q

Von Willebrand Disease

A

Most Common Inherited Bleeding Disorder; 1% Prevalence in US; Most are Asymptomatic

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10
Q

Major Functions of von Willebrand Factor

A

Binds Factor VIII & Extends Life of F VIII
Binds Platelets to Injured Vessel Endothelium
Helps to Insure that Coagulation & Healing take place at site of Vessel Injury

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11
Q

Clinical Presentation of von Willebrand Factor

A

Mucosal Bleeding including Epistaxis & After Dental Extractions
Post Op Bleeding
Metromenorrhagia

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12
Q

Von Willebrand Factor are stored in what?
production stimulated by what?
release is stimulated by what?

A

Stored in Vessel Endothelial Cells and Platelets
Its Production is Stimulated by Estrogen and T4
Its Release is Stimulated by Vasopressin, Epinephrine, Histamine & Thrombin
Ultra-large Multimers are Broken Down by the Enzyme ADAMTS-13
Too Many Ultra-Large Multimers in the Circulation Will Causes Pathological Clotting: TTP

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13
Q

Type 1 Von Willebrand Disease Labs and Treatment

A

Most Common
Autosomal Co-Dominant
Normal Distribution of Multimers; Decreased Quantity vWF
decreased vWAg, decreased vW F Activity, decreased F VIII Activity
Responds to DDAVP
DDAVP can be given as Nasal Spray or IV

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14
Q

Type 2 a, b & m

Von Willebrand Disease

A 
Qualitative Abnormalities in vWF or Abnormal Distribution of Multimers
Type 2b ( excessively big multimers) can be associated with Thrombocytopenia and should NOT Be Treated with DDAVP as this can WORSEN Thrombocytopenia and even precipitate abnormal clotting.
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15
Q

Some Tests of Clotting Useful in Diagnosing von Willebrand Disease?

A 
Von Willebrand Factor Antigen
vW Factor Activity
Von Willebrand Factor Multimers
Bleeding Time
Factor VIII Activity
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16
Q

Epidemiology of Hemophilia A

A

X-Linked recessive, therefore severe Sx only in Males
Deficiency of Factor VIII; 1: 5,000 in population
Usually Manifest as Easy Bruising or Bleeding particularly Hemarthoses in Male Toddlers.

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17
Q

Hemophilia A Treatment?

A

Treated with Recombinant Factor VIII Replacement IV as Rx’d by a Hematologist
If Patient born Before 1985 , Hepatitis & HIV were Major Risks
Prophylactic Rx is Desirable
After Prolonged Rx, Inhibitors can Form: A Big Problem
Management Should Strive to Avoid Painful Joint Bleeding & Deformity

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18
Q

Hemophilia B:

A

Deficiency of F IX
X-Linked recessive, therefore severe Sx only in Males
Clinically Identical to Hemophilia A
1: 30,000
Treated with Recombinant Factor IX Concentrate which can be Pro-thrombotic

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19
Q

Factor XI Deficiency epidemiology

A

Autosomal Co-dominant
Family Hx Usually +
Rare in the General Population, but Heterozygotes may be present in as many as 6% of the Jewish Population.
Only few are Sx’ic and most present in Adulthood as Heterozygotes have Mild Sx
Sx Similar to Hemophilia
Usually Rx’d with Fresh Frozen Plasma (FFP)

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20
Q

Vitamin K absorbed?

A

Vitamin K is a fat soluble vitamin absorbed through the gut.

Most of the Vitamin K we absorb is the result of either bacteria in our gut or from plant materials.

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21
Q

Vitamin K is important because?

A

Vitamin K is essential for the Post-translational activation of many proteins, particularly Clotting Factors II ( Prothrombin),VII,IX & X.
Vitamin K also actives the Anti-thrombotic Proteins C & S

22
Q

Coumadin

A

Coumadin® (warfarin) is a Vitamin K Antagonist that works by Inhibiting Vitamin K Reductase. The Reduced Form of Vitamin K is the Active Form.
Coumadin® is metabolized by enzymes of the Cytochrome Family found in the liver, mostly CYP2C9, which has a variety of genetic variants, e.g. CYP2C92 & CYP2C93.

23
Q

Vitamin K Dependent Clotting Factors

A

The T1/2 of Factor VII is 4 hours.
The Physiologic Anti-Coagulant Effects of Coumadin® Depend on Lowering Levels of Factor II (Prothrombin) and Factor X.
Therefore when Coumadin is Started one may Falsely Sense the the Patient is Anticoagulated when he is NOT.
Conversely When Coumadin is Stopped, one may Falsely think that the Anti-coagulant Effect of Coumadin is gone, when it is NOT.

24
Q

Coagulopathy of Kidney Disease

A

More Mild than that of Liver Disease, but Can be Associated with an Increased Tendency for Both Thrombosis and Bleeding.
Restoring Renal Function with Dialysis or Other Measures is Important.
FFP and Sometime Platelet Transfusion are Helpful.

25
Q

Disseminated Intravascular Coagulation (DIC)

A

Symptom of Other Pathological Process, a Syndrome.
The Clinical Hallmark of this Syndrome is Diffuse Bleeding frequently from Mucosal Sites, Sites of Previous Surgery or Instrumentation and Organ Failure d/t Thromboses.

26
Q

The Causes or Clinical Scenarios in Which One Might See DIC

A

Metabolic
Infectious
Neoplastic
Immune/Inflammatory/ Injury

27
Q

5 Immune/Inflammatory/ Injury that cause DIC

A

Brain Injury
Fat or Amniotic Fluid Embolus
Abrutio placentae
Severe Pre-eclampsia or HELLP Syndrome ( Hemolysis, Elevate LFTs, & Low Platelets)

28
Q

Labs for DIC

A

Micro-angiopathic Hemolytic Anemia
Thrombocytopenia
DIC and TTP can share some Characteristics, BUT in TTP the PT & aPTT should be Normal and FDPs should be Normal or nearly Normal

29
Q

How do you treat DIC

A

First Treat the Underlying Cause of the DIC!
Next Think about Replacing Clotting and Anti-clotting Factors with FFP.
Use Platelet Transfusions Sparingly
Treatment with Anti-coagulants is Risky

30
Q

Heparin and Other Clotting Factor Inhibitors

A

Unfractionated Heparin is a sulfated polysaccharide of various Molecular Weights mostly derived from porcine intestine.
Heparin Functions by Accelerating the Action of Antithrombin.
Antithrombin has its Most Significant Biological Impact by Inhibiting Factor Xa.

31
Q

What is Low Molecular Weight Heparin?

A

is Synthesized from Unfractionated Heparin. It is dosed based on the Patient’s Weight. No monitoring is Routinely Done; One Can Measure Anti-Xa Activity. Normal Renal Function is Important for the Rx of LMWH.

**HIT less likely

32
Q

Unfractionated Heparin Activity is Generally measured how?

A

Generally Monitored by Measuring the aPTT. Therapeutic: 2 -3 x Normal

33
Q

Fondaparinux is?

A

synthetic polysaccharide that also binds to Antithrombin and Functions Like Heparin as an Antithrombin Accelerator.
only Approved for Deep Venous Thrombosis (DVT) Prophylaxis

34
Q

Dabigatran ( Pradaxa® )

A

an Oral Direct Thrombin Inhibitor. It is Approved for Prophylaxis of Stroke in Patients with Atrial Fibrillation.

35
Q

Aspirin high doses

A

Higher Doses Aspirin (ASA) Inhibits both COX 1 & 2, Lowering Levels of the Anti-thrombotic Protein, Prostacyclin as well as Other Inflammatory Proteins.

36
Q

ASA low doses

A

Anti-thrombotic dose of ASA is 85 -325 mg p.o. Q Day.
Since this drug irreversibly binds COX1, it’s effects last for the life of the Platelet, ~ 7 Days.
Higher doses are NOT Effective as Anti-platelet Rx

37
Q

Plavix® (clopidogrel)

A

The Oral Inhibitors of P2Y12

Indicated for Use with ASA to Lower Risk of Stroke or MI, after coronary stenting or recent MI.

38
Q

GPIIb/IIIa

A

is an Adhesion Receptor on Surface of Platelets. In its active form it Binds Fibrinogen and vWF.
(abciximab) (eptifibatide).
Administered Intravenously

39
Q

GPIIb/IIIa indicated in what?

A

Indicated in Acute MI when patients are Undergoing Coronary Stenting

40
Q

What is the Most Common Inherited Hypercoaguable State is Due to

A

Factor V Leiden ( VL)

41
Q

Treatment of Factor VL

A

Asymptomatic Carriers: Education about Increased Risk Situations
Patients with Factor VL in High Risk Situations should be Rx’d with Anti-coagulation till that Situation is Resolved
Patients with > One Previous DVT or PE: Anticoagulation Probably for Life

42
Q

Prothrombin Gene Mutation G20210A

A

Second Most Common Inherited Hypercoaguable State
Autosomal Co-dominant
Results in Increased Plasma Levels of Prothrombin

43
Q

Situational Risk Factors (Transient) for hypercoaguable states

A 
HIT
Surgery
Sepsis
Immobilization
BCPs or Pregnancy
HRT
Inflammatory States d/t  Factor VIII
44
Q

Acquired Risk Factors (More Permanent) hypercoaguable states

A 
Inflammatory Bowel Disease
Portal Hypertension
Cancer & Cancer Chemotherapy
Nephrotic Syndrome
Anti-Phospholipid Antibody Syndrome
45
Q

Treatment of Antiphospholipid Antibody Syndrome

A

Routine Rx of Thrombosis with Heparin and Coumadin are Appropriate
Monitoring and Proper Dosage may be Difficult as Baseline aPTT and Occasionally PT may be Abnormally Elevated
Immuno-suppressive Rx and ASA May have a Role

46
Q

Clotting Problems Can Be Divided Into

A

Problems of the Vessel Walls (We Did Not Discuss These in Detail)
Problems with the Soluble Clotting Factors
Problems with The Soluble Anti-clotting Factors
Problems with Platelet Discussed Here and in the Thrombocytosis Lecture and the Thrombocytopenia Lecture
Problems with a Mixture of the Components of the Clotting System

47
Q

3 Problems of the Vessel Walls

A

Vessel Injury
Atherosclerosis
Vessel malformation

48
Q

3 Problems with the Soluble Clotting Factors

A

Factor Deficiencies: VIII, IX, vWF
Factor Inhibitors: anti-Factor VIII
Overactive Clotting Factors: VL or Prothrombin Mutation

49
Q

5 Problems with The Soluble Anti-clotting Factors

A 
Deficiency of Protein C &S 
			Coumadin
			Anti-phospholipid Syndrome
		Augmentation of Anti-Thrombin
			Heparin
50
Q

3 Mixed Coagulopathies

A

DIC
Coagulopathy of Liver Disease
Coagulopathy of Kidney Disease

Clin Med- Heme/Oncol (10 decks)

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