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75 Cards in this Set

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Thrombocytopenia
Decreased platelet count resulting in bleeding
Thrombocytosis
Increased platelet count
One cause of hereditary thrombocytopenia?
May Hegglin anomaly (autosomal dominant)
Two causes of abnormal hematopoiesis (acquired)?
1. B12/folate deficiency
2. pre-leukemic state
What are five causes of drug induced thrombocytopenia?
Heparin, gold, quinine, sulfonamides, GP IIb/IIIa inhibitors
VIP

Explain what happens in heparin induced thrombocytopenia?
Heparin binds to PF-4 to form a complex that induces pathologic antibody formation. This causes thrombocytopenia (decrease in the # of circulating platelets) by activating platelets. However, at the same time it is using those platelets randomly to form clot (high risk of thrombosis)
What is can GPIIb/IIIa inhibitors cause?
drug induced thrombocytopenia
VIP VIP VIP

ITP and TTP cause systemic thrombocytopenia: How?
ITP: Immune thrombocytopenic purpura, caused by IgG antibodies that target IIb/IIIa or Ib-9 causing bleeding.

TTP: thrombotic thrombocytopenic purpura, caused by an inability to cleave the vWF away from a thrombus. Causes arterial thrombi and has neural manifesations. Platelets with out trigger start clumping together
Where is the Platelet factor 4 that is made?
Platelet: light granules
VIP

Explain what happens in heparin induced thrombocytopenia?
Heparin binds to PF-4 to form a complex that induces pathologic antibody formation. This causes thrombocytopenia (decrease in the # of circulating platelets) by activating platelets. However, at the same time it is using those platelets randomly to form clot (high risk of thrombosis)
What is can GPIIb/IIIa inhibitors cause?
drug induced thrombocytopenia
VIP VIP VIP

ITP and TTP cause systemic thrombocytopenia: How?
ITP: Immune thrombocytopenic purpura, mediated
Where is the Platelet factor 4 that is made?
Platelet: light granules
What is HUS?
Hemolytic uremic syndrome: just like TTP but with out CNS problems
What is thrombocytosis?
increase number of circulating platelets
What are three conditions that can lead to thrombocytosis?
1. spleenectomy - thrombocytosis eventhough platelets are normal
2. Reactive thrombocytosis - caused by cancer, infection, drugs, iron def
3. Autonomous thrombocytosis clonal disorder - platelet number is very high naturally can cause thrombosis.
What can a diet high in omega-3-fatty acids cause?
reduced platelet function
VIP VIP VIP

What is Glanzmann's Thrombasthenia?
An autosomal recessive disorder in which there is defective GP IIb/IIIa (no fibrinogen bridge can occur)resulting in aggregation defects and increased bleeding time.
VIP VIP VIP

What is Bernard-Soulier disease?
Autosomal recessive disorder with a defect in GP Ib causing platelets to be unable to anchor to vWF leading to no formation of primary platelet plug thus increasing bleeding time.
What happens in the storage pool disease?
There is a decrease in dense granular content of platelets inhibiting aggregation.
What is non-thrombocytopenic purpura?
A disorder that does not result in severe bleeding diathesis since coagulation is normal, patients just bruise easily.
What is Ehler-Danlos syndrome?
Hypermobile jts from a defect in collagen synthesis
What is telangiectasia?
spider veins
What does a PT test?
Extrinisic pathway:7, 10, 5, 2 and fibrinogen
What does an aPPT test?
Intrinsic pathway: 12, 11, 9, 8, 10, 5, 2 (all factors except 7, 13, protein C and S
Under what three diagnostic conditions do you run an aPPT?
When you suspect hemophilia A or B or the patient is on Heparin.
In a patient with Hemophilia what kind of value would you except on an aPPT?
High
VIP

Describe Hemophilia A (classical):
F 8 deficiency that stops the bodies ability to clot and increases bleeding tendency. Symp: bleeding in jts and m.
Describe Hemophilia B (x-mas disease)
F 9 deficiency, same symp as Hemo A
VIP

What is vonWilledebrand disease?
Adhesion defect due to vWF defects. Can't form primary plug thus an increase in BLEEDING TIME (BT) and a slightly elevated APTT.
What happens in a patient with Activated Protein C resistance?
Since protein C normally cleaves 8a and 5a to inhibit clotting this resistance causes a longer generation of thrombin and leads to a hypercoaguable state.
What goes wrong in Dead Fetus Syndrome?
Massive amount of fibrinogen are degraded and so clots can not be formed.
What happens in some snake bites? Similar to what syndrome?
Fibrinogen is degraded just as in Dead Fetus Syndrome
VIP VIP VIP

Explain secondary fibrinolysis (disseminated intravascular coagulation)
Both fibrin and fibrinogen are digested by plasmin resulting in a simultaneious digestion of clotting factors and consumption of platelets.
What is the main cause of DIC?
Sepsis (overwhelming infection of blood stream produced by toxin-producing bacteria)
VIP

What does sepsis cause the release of? What does this cause?
Tissue factor!!! Causing widespread thrombosis
VIP

What is caused from a deficiency of alpha-2 antiplasmin?
Since antiplasmin inhibits plasmin thus inhibiting clot breakdown. A deficiency of this inhibitor causes an increase in clot breakdown = increase in bleeding.
nL

What three things are immediately released when a blood vessel is damaged?
1. endothelin - vasoconstriction
2. NO
3. prostacylin - both are released to cause vasodilation and prevent clots
nL

After a blood vessel is damaged primary hemostasis occurs. Describe this process:
Platelet adhesion occurs from the exposed collagen of the endothelium.
Platelets are then activated, changing shape, and releasing their granules.
nL

Where is vWF produced?
Constituitively in the endothelium
nL

After a blood vessel is damaged secondary hemostasis occurs. Describe:
Tissue factor is released immediately at site of injury from endothelial cells. This produces a coag cascade that results in the formation of thrombin and thus fibrin. Therefore secondary hemostasis is responsible for forming a STABLE clot via COAGULATION.
nL

Three things thrombin does:
1. stimulates recruitment of additional platelets
2. stimulates activation of additional platelets
3. converts fibrinogen to fibrin
nL

After clot is fully formed what two things are released?
1. t-PA (tissue plasminogen activator) - for fibrinolysis; forms plasmin

2. thrombomodulin - binds with thrombin to activated protein C. Protein C lysis 8a and 5a
nL
How to antithrombins (anticoagulant medications) mediate their effect?
Antithrombins bind with heparin-like molecules and inactivate thrombin (2a) and 9a, 10a.
nL
How does the left over thrombin floating around get inactivated and end up helping to stop coagulation cascade?
Thrombin can bind to a thrombomodulin receptor forming a complext that activated protein C which lysis 8a and 5a
nL
What do normal endothelial cells secrete to prevent platelet aggregation?
NO, prostacyclin, PGI2, ADP
nL
What produces "heparin-like" molecules?
Endothelial cells
Where are thrombomodulin receptors (VIP) located?
On the endothelial cells
nL

What is the function of the PGI2, NO, and ADP that the endothelial cells release?
To inhibit platelet aggregation
nL

How does the presence of fat on the walls of the arteries change the vessels responses?
fat inhibits antithombotic mechanisms
nL

What do infections do to the characteristics of the blood?
Slow blood down, produce plasma lipids, and ischemia (change endothelial cell function)
nL

What three diseases exhibit prothrombotic states?
1. diabetes
2. CHF
3. hypervisocosity syndrome
nL - VIP

What do light granules contain? Dark?
Light: fibrinogen, fibronectin, coag factors 5 and 8, platelet factor 4, growth factors, PDGF, TGF-beta

Dark: ADP, ATP, Ca, histamine, serotonin (VIP), epinephrine
nL

What does platelet factor 4 do when released?
Neutralizes heparin
nL

What does serotonin do when released by platelets?
Vasoconstricts
nL

How are platelets activated? What happens once they are activated?
To activate: Platelets molecules must bind to their GPIIa/IIIb receptors forming a fibrinogen bridge.

Once activated they release their granules and activate other phospholipids on platelets to expose their GPIIb/IIIa
nL
VIP!!
What happens at the GP IIb/IIIa site?
Here coagulation factors combine with ionized Ca (from dense granules) to activate the intrinsic pathway to form thrombin
nL

What forms the primary hemostatic plug? Secondary?
Primary: release of ADP and thromboxane A2 from platelets - recruits other platelets to form plug

Secondary: Fibrin from coag cascade surrounds platelets forming this irreversible plug.
nL

What is released during an MI that increases thrombosis formation? What is given to these patients to combat this?
Released: massive amounts of thromboxane A2 - accelerates platelet aggregation.

Give: t-PA - lyse clots
nL

What pathway does Heparin inhibit?
Intrinsic
nL

How is the effect of Warfarin measured?
using PT (measure inhibition of factor 7)
nL

Which factor is: Prothrombin?
2
nL

Which factor is: Proconvertin?
7
nL

Which factor is: Stuart factor?
10
nL

Which factor is: Hageman factor?
12
nL

Which factor is: Fibrin stabilizing factor
13
nL

Fibrinogen group of factors:
1, 5, 8, 13
nL

Prothrombin group of factors:
2, 7, 9, 10
nL

Describe how inhibitors of the coagulation system work?
These inhibitors are plasma proteins which are capable of inhibiting the formed serine protease enzymes involved in the regulation of the clotting process
nL

What are two inhibitors of the coagulation system?
1. antithrombin III - inactivates enzymes of coagulation system

2. tissue factor pathway inhibitor
nL

What three things are responsible for the anticoagulation effects of heparin?
1. antithrombin
2. heparin
3. tissue factor pathway inhibitor
nL

Function of the fibinolytic system?
Dissolve clots using proenzymes like plasminogen activator.
nL

What is Plasminogen activator inhibitor do and in what condition is it upregulated?
Decreases bodies ability to lyse clots. Diabetes has an upregulation of this PAI.
nL
VIP
What does alpha-antiplasmin do?
It inhibits formed plasmin - threre for inhibiting clot breakdown
nL
VIP VIP VIP

What is Virchow's Triad?
Three major factors that contribute to thrombosis:
1. injury to endothelium
2. alterations in blood composition and flow
3. stasis