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Block 2 Pathophysiology > Hematology- hemostasis > Flashcards

Hematology- hemostasis Flashcards

1
Q

The processes which
Allow blood to remain fluid in vessels
Form a hemostatic plug at sites of vascular injury

A

Hemostasis

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2
Q

___when the thrombus forms at one place and travels to a distant site

A

Embolus

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3
Q

____ at the site of intravascular coagulation

A

Thrombus

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4
Q

Hematoma,Purpura, Ecchymoses,Petechiae are examples of ____

A

Bruising: bleeding into or beneath the skin

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5
Q

Signs and symptoms of defective hemostasis

A

Bruising: bleeding into or beneath the skin
Mucosal bleeding
Menorrhagia: heavy, prolonged menstrual bleeding at regular intervals

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6
Q

_____ is heavy, prolonged menstrual bleeding at regular intervals

A

Menorrhagia

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7
Q

types of Mucosal bleeding

A

Epistaxis: “nose bleed”
Hematemesis: vomiting blood
Hemoptysis: coughing up blood
Hemarthrosis: bleeding into joint capsules

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8
Q

______is normally antithrombotic

A

Endothelium

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9
Q

Endothelial factors with antiplatelet actions

A

Prostacyclin (PGI2)
Nitric oxide (NO)
Adenosine diphosphatase

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10
Q

Endothelial factors with anticoagulant actions

A

Heparin-like molecules work with antithrombin III (liver) to inactivate thrombin, factor Xa and others

Thrombomodulin converts thrombin from procoagulant to anticoagulant

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11
Q

_____ work with antithrombin III (liver) to inactivate thrombin, factor Xa and others

A

Heparin-like molecules

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12
Q

_______ converts thrombin from procoagulant to anticoagulant

A

Thrombomodulin

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13
Q

Endothelial factors with fibrinolytic actions

A

Tissue plasminogen activator (tPA)

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14
Q

Endothelial injury (activation) favors ____

A

thrombosis

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15
Q

Endothelial factors with pro-platelet aggregation actions

A

Von Willebrand factor (vWF)

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16
Q

this is Cofactor for platelet binding to collagen

Produced by activated endothelial cells

A

Von Willebrand factor (vWF)

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17
Q

Endothelial factors with pro-coagulation actions

A

Tissue factor

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18
Q

this is Produced in response to cytokines and endotoxin

Activates the extrinsic clotting cascade

A

Tissue factor

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19
Q

Endothelial factors with pro-fibrin activation

A

Inhibitors of plasminogen activator (PAI)

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20
Q

this Inhibit fibrinolysis

A

Inhibitors of plasminogen activator (PAI)

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21
Q

Bleeding Disorders May be caused by failures in

____

A

Primary hemostasis–>Platelet deficiency or dysfunction

Secondary hemostasis–>Dysfunction in the coagulation system

Combination

22
Q

Primary Hemostasis: Platelets

A 
Form platelet plug in porous vessels
Activate blood coagulation (secondary hemostasis)
Support endothelium
Secrete cytokines
Lifespan 5-10 days
Removed by spleen 
    and liver
23
Q

Platelets: exposure to ADP, collagen, thrombin favors activation and results in the following

A
  1. Adherence to collagen and activation by von Willebrand factor (vWF)
  2. Shape change to increase clumping- Exposes phospholipid complexes which activate the intrinsic coagulation pathway (secondary hemostasis)
  3. Secrete pro-aggregatory granule products (e.g., ADP) and thromboxane A2 (TXA2)
  4. Activate (recruit) other platelets
  5. Produce primary hemostatic plug
24
Q

Primary Hemostasis: Platelet Adhesion

Step 1: Adherence

A 
Activated (injured) endothelial cells secrete von Willebrand factor (vWF)
When basement membrane 
   collagen is exposed, vWF 
   binds to collagen and 
   platelets bind to vWF 
   (platelet Gp1b and Gp2b3a 
   receptors), forming plug
25
Q

Primary Hemostasis: Platelet Shape

Step 2: Activation and shape change

A

The first step in platelet activation results in shape change in two steps

  • Calcium influx activates cleavage of actin filaments, causing the cell to become spherical
  • Actin reassembles in linear form making spicules
  • Calcium influx also activates phospholipases, modifying membrane phospholipids (secondary hemostasis)

Shape change promotes platelet aggregatio

26
Q

Primary Hemostasis: Granule Release

Step 3: Degranulation

A

Initiated by calcium influx which causes shape change
- Delta granules contain ADP, calcium, serotonin, epinephrine
ADP and calcium supports recruitment of more platelets
Serotonin and epinephrine results in vascular constriction
- Lambda and Alpha granules contain
lytic enzymes, growth factors, etc.
- Pro-thrombotic thromboxane
(TXA2) produced from membrane
phospholipids
- Healthy endothelial cells secrete
anti-thrombotic prostacyclin (PGI2),
blocks platelet degranulation

27
Q

Primary Hemostasis: Platelet Recruitment

Step 4: Recruitment of more platelets

A

ADP (from delta granules) and TXA2 (membrane phospholipid metabolism) enlist more platelets to undergo the same processes, perpetuating platelet aggregation

28
Q

Platelet adhesion to collagen is mediated by endothelial cell _________.

A

von Willebrand factor

29
Q

Platelet aggregation results in release of ADP (enhances aggregation) and phospholipid complex (initiates intrinsic clotting pathway), resulting in _________.

A

fibrin deposition

30
Q

Together the aggregated platelets and fibrin form a ______.

A

hemostatic plug

31
Q

______ defined as platelet count below 150,000 platelets/μL (normal range, 150,000/μL to 400,000/μL)

A

Thrombocytopenia

32
Q

Spontaneous bleeding rarely occurs until platelet counts fall below _____

A

20,000 platelets/μL

33
Q

Platelet counts from 20,000 to 50,000 platelets/μL can aggravate _____

A

post-traumatic bleeding

34
Q

Bleeding episodes usually involve small vessels in ________(petechiae, purpura), risk of intracranial bleeding

A

skin and mucous membranes

35
Q

Bleeding resulting from ______ is associated with a normal PT and PTT (measures of secondary hemostasis)

A

thrombocytopenia

36
Q

Platelet Disorders: Thrombocytopenia

Four primary causes

A

Decreased platelet production
Sequestration
Dilution
Decreased platelet survival

37
Q

Decreased platelet production

A

Depressed marrow output (e.g., aplastic anemia and leukemia)
Certain drugs and alcohol, HIV, myelodysplastic syndromes

38
Q

Sequestration

A

The spleen normally sequesters 30% to 35% of the body’s platelets, but this can rise to 80% to 90% with splenomegaly, producing moderate degrees of thrombocytopenia

39
Q

Dilution

A

Massive transfusions with platelet-poor plasma, packed RBC, or crystalloid fluids can produce a dilutional thrombocytopenia

40
Q

Decreased platelet survival

A

Immune thrombocytopenia caused by auto- or allo-antibodies to platelets

Nonimmune thrombocytopenia caused by uncontrolled, systemic platelet activation or destruction

41
Q

Functional disorders of platelets

hereditary

A

Adhesion defects
Aggregation defects
Release defects

42
Q

Functional disorders of platelets

Iatrogenic disorders

A 
ADP receptor inhibitors 
Gp2b3a antagonists
Phosphodiesterase inhibitors
Thrombin receptor blockers
Cyclooxygenase / thromboxane inhibitors
Adenosine reuptake inhibitors
43
Q

Most common inherited bleeding disorder in humans (1% population)

A

Von Willebrand’s Disease

44
Q

Majority of Von Willebrand’s Disease cases are ______.

May be acquired or associated with other conditions (malignancy, immunologic responses, drugs, miscellaneous disorders)

A

autosomal dominant

45
Q

Von Willebrand’s Disease presentation

A

Symptomatic at any age
Epistaxis in childhood
Easily bruised especially with sports
Excessive bleeding with surgical procedures
Heavy menstrual (menorrhagia) and peripartum bleeding
May be history of bleeding after use of ASA or NSAIDS

46
Q

what is Antiphospholipid syndrome (autoimmune)

A

Aggregation defect where antiphospholipid autoantibodies result in platelet coagulation

47
Q

what is Antiphospholipid syndrome (autoimmune) is Associated with

A

Associated with
Recurrent arterial and venous thrombosis (50%)
Repeated fetal loss
Thrombocytopenia

48
Q

Secondary hemostasis is associated with _____ and their activation

A

clotting factors

49
Q

____is a required cofactor for prothrombin

A

Vitamin K

50
Q

___ is principal initiator of intrinsic pathway

A

Collagen

51
Q

Secondary Hemostasis Process accelerated by

A

Factor VIIa (extrinsic pathway )
Thrombin (common pathway)
Activated platelet membrane phospholipids (primary hemostasis)

52
Q

Secondary Hemostasis Process intrinsic pathway ends in

A

Ends in activation of factor X to factor Xa

Block 2 Pathophysiology (8 decks)

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