Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
75 Cards in this Set
- Front
- Back
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 |