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Drug Action I > Block 3 - Hemostasis Phys > Flashcards

Block 3 - Hemostasis Phys Flashcards

1
Q

What is hemostasis?

A

Cessation of blood flow by coagulation mechanisms

Used to stem hemorrhage

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2
Q

What is the difference between hemorrhage and ecchymoses?

A

Hemorrhage: copious bleeding

Ecchymoses: bruising, bleeding of the skin

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3
Q

What can disorders of hemostasis lead to?

A

Excessive coagulation or bleeding

Genetic errors → problems with thrombocyte (platelets) number or function

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4
Q

What are the steps of hemostasis?

A
  1. Vascular phase (initiation)
  2. Aggregation phase (amplification)
  3. Coagulation phase (propagation)
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5
Q

What occurs in the vascular phase?

A
  1. Spasm of BV
  2. Platelets activated and travel to site of injury
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6
Q

What occurs in the aggregation phase?

A
  1. Continued platelet activation
  2. Platelets clump and form a plug
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7
Q

What occurs in the coagulation phase?

A

Platelets release substances that lead to formation of fibrin layer over the platelet plug

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8
Q

What is primary disorders? Example?

A

Abnormalities in platelet number or function or thrombocytopenia

von Willebrand disease

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9
Q

What are secondary disorders? Examples?

A

Lack of or reduction in factors tied to coagulation results in genetic factors

Hemophilia
Vitamin K deficiency

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10
Q

What is Thrombocytopenia vs Thrombocythemia?

A

Penia: low platelets
Cythemia: Excess of platelets

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11
Q

What are examples of hereditary disorders?

A

von Willebrand disease, hemophilia

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12
Q

What are examples of acquired disorders?

A

issues related to vitamin K utilization, liver disease

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13
Q

What does the immune system play a role in hemostasis?

A

Regulation of coagulation

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14
Q

What is the the liquid portion of the blood? Portion of TBW? Components?

A

Plasma: 55%

Water
Plasma protein
Miscellaneous molecules

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15
Q

What are the formed elements? Portion of TBW? Components?

A

Blood cells: 45%

Erythocytes
Leukocytes
Thrombocytes

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16
Q

What is hematopoiesis?

A

Process by which blood cells are formed

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17
Q

What cells produce new blood cells? What causes its proliferation and differentiation?

A

Hematopoietic stem cells (HSCs)

growth factors and immune mediators

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18
Q

What do HSCs differentiate into? Function?

A
  1. Lymphoid precursor cells: Divide to produce lymphocytes
  2. Myeloid precursor cells: Divide to produce RBS, granulocytes, monocytes, and megakaryocytes
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19
Q

What are Megakaryocytes?

A

Large cell in the bone marrow responsible for production of thrombocytes (platelets)

Megakaryocytopoiesis

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20
Q

What regulates thrombopoiesis?

A

Cytokines and growth factors

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21
Q

What is the most important growth factor in platelet production? Why?

A

Thrombopoeitin

  1. Stimulates proliferation of platelets and progenitor cells
  2. Suppor differentiation of megakarytocytes
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22
Q

As platelets increase, thrombopoeitin (increase/decrease)?

A

Decrease

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23
Q

What is IL-3?

A

Growth factor that supports early development of progenitor cells.

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24
Q

What is IL6?

A

Growth factor that acts in synergy with thrombopoietin to increase numbers of megakaryocytes

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25
Q

What is IL-11?

A

Growth factor that stimulates platelet production by acting on early progenitor cells and in the development of megakaryocytes

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26
Q

What are coagulation pathways of hemostasis?

A

Intrinsic pathway
Extrinsic pathway

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27
Q

What activates the intrinsic pathway?

A

Damage within vascular system

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28
Q

Describe the mechanisms of intrinsic pathway?

A
  1. Activation of proenzymes exposed to collagen fibers at site of injury.
  2. Assistance of PF-3 (factor released by aggregating platelets).
  3. After a series of linked reactions, activated clotting factors combine to form an enzyme complex capable of activating factor X.
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29
Q

What activates extrinsic pathway?

A

Presence of blood outside the standard circulating system

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30
Q

What are the mechanisms of extrinsic pathways?

A
  1. Release of tissue factor (TF; also called factor III) by damaged endothelial cells or peripheral tissues
  2. Tissue factor combines with Ca2+ and another clotting factor to form an enzyme capable of activating factor X
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31
Q

What is a common pathway? How does it begin?

A

A set of components shared by the intrinsic and extrinsic

Activated factor X

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32
Q

What are the mechanisms of common pathway?

A
  1. Activated factor X activates a complex called prothrombin activator. (Phase 1)
  2. Prothrombin activator converts the proenzyme prothrombin into the enzyme thrombin. (Phase 2)
  3. Thrombin completes the clotting process by converting fibrinogen to fibrin. (Phase 3)
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33
Q

What is the center of primary disorders?

A
  1. Platelet function and binding.
  2. Considerations related to integrity of vascular endothelial cells
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34
Q

Types of primary disorders?

A

von Willebrand disease (vWD)

Thrombocytopenia

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35
Q

What is the most common genetic bleeding disorder?

A

vWD

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36
Q

Wha is wWF?

A

allowing platelets to adhere to points of injury

37
Q

What is vWF compared to ADAMTS13?

A

vWF glue seals a bleeding wound by helping to trap platelets

ADAMTS13 trims away excess glue

38
Q

What is T1vWD?

A

Most common case?

Failure to make enough or increased clearance

39
Q

What is T2vWD?

A

Impairment or enhanced binging ability

40
Q

What is T3vWD?

A

Most sever

Absence of production of vWF

41
Q

What vWD is mostly asymptomatic?

A

T1

42
Q

What vWD presents much like hemophilia?

A

T3

43
Q

What are the treatments of vWD? What types do it treat?

A
  1. Desmopressin (T1 and T2 subset)
  2. Transfusion with plasma-derived vWF products (factor VIII and vWF) : (type 3 vWD and with type 2 vWD when DDAVP is ineffective)
44
Q

What is the normal range for platelets? Increased? High risk bleed?

A

150,000-45,000

80,000 – 100,000

<10,000

45
Q

What are the pathophysiologic processes of thrombocytopenia?

A

1.Pseudothrombocytopenia
2. Deficient platelet production
3. Increased destruction and/or consumption of platelets
4. Abnormal distribution or pooling of platelets

46
Q

What causes psuedothrombocytopenia?

A
  1. false thrombocytopenia
  2. caused by platelet clumping secondary to use of EDTA
47
Q

How can deficient platelet production → thrombocytopenia?

A

Produce marrow aplasia

Bone marrow replacement can de a cause to

48
Q

Most common cause of drug-induced deficits in platelet production?

A

Heparin

49
Q

What is T1HIT?

A

Involves modest decrease in platelet count within first 2-3 days of heparin therapy → return to normal

50
Q

What is T2HIT?

A

Caused by antibodies to platelet factor 4 on the heparin complex → systematic in 4-14 days

51
Q

What factors increase the destruction/consumption of platelets?

A
  1. Immune thrombocytopenic purpura (ITP)
  2. Thrombotic thrombocytopenic purpura (TTP)
52
Q

What is immune thrombocytopenic purpura? Where does it occur?

A

Autoimmune disease that involves the destruction of platelets by anti platelet antibodies → relapses and remits

Spleen, wound adult females

53
Q

What is Thrombotic thrombocytopenic purpura (TTP)?

A

Deficiency or absence of protease called ADAMTS13

54
Q

What happens to ADAMTS13 with TTP?

A

Low or absent level, vWF can unfold without vessel injury → formation of platelet thromboses

55
Q

What causes pooling of platelets? Is it reversible?

A

Uncomplicated splenomegaly or hypersplenism

Yes

56
Q

What is the most common cause of splenic pooling?

A

Chronic liver disease with portal hypertension and congestive splenomegaly

57
Q

Where does most bleeding take place?

A

Mucocutaneous

58
Q

What is purpura?

A

Tiny pinprick hemorrhages on skin

59
Q

What is ecchymoses?

A

Discoloration of the skin resulting from bleeding underneath, typically caused by bruising; arise after relatively minor trauma

60
Q

What is epistaxis?

A

Nose bleed

61
Q

What are the clinical manifestation of thrombocytopenia (TTP)?

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. Renal insufficiency
  4. Fever
  5. Mental status changes that can wax and wane
62
Q

What are the treatments of thrombocytopenia?

A
  1. plasmapheresis
  2. Infusion of fresh frozen plasma
63
Q

What is plasmapheresis?

A
  1. Plasma separated from blood cells and re-infused with another solution
  2. TTP
  3. Reduces autoimmune antibody concentration → slowing platelet destruction
64
Q

What are examples of inherited?

A

Hemophilia (can be acquired)

65
Q

What are acquired?

A

deficiencies in Vitamin K

66
Q

What is Hemophilia A and B?

A

A: Lack of factor VIII
B: Deficiency in factor IX

Both chromosomal abnormalities

67
Q

What is hemophilia?

A

Hereditary genetic bleeding disorder

68
Q

What are causes of acquired hemophilia?

A
  1. Autoimmune disease
  2. Cancer
  3. Pregnancy

development of factor VIII and factor IX inhibitors

69
Q

Clinical manifestations of hemophilia?

A
  1. Bleeding → inability to clot
  2. Significant bleeding in tissues
  3. Circumcision
  4. Bleeding in tongue and gums
70
Q

What hemophilia is most common?

A

B

71
Q

What population is primarily affected by hemophilia?

A

Males from mothers X chromosome

72
Q

What are the treatments for hemophilia?

A

Episodic or prophylactic administration of factor VIII or factor IX concentrates however some patients can develop inhibitors to clotting facotrs

73
Q

What is sickle cell?

A
  1. Affects the clotting pathways
  2. Procoagulation
74
Q

What are the clinical manifestations of sickle

A
  1. Clumping → obstructed BF, hypoxia, tissue ischemia
  2. Tissue ischemia → pain
  3. Frequent thrombosis → strok
75
Q

What are the signs of ischemic damage?

A
  1. Swelling
  2. Tenderness
  3. Rapid RR
  4. HTN
76
Q

How is sickle cell diagnoses?

A

Increase concentration of thrombin and loss of anticoagulant proteins

77
Q

What is the treatment for sickle?

A

1 Reduce platelet binding
2. Inhibit platelet activation

78
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

Proteins that control clotting become overactive where clotting factors are consumed and spontaneous bleeding

79
Q

What can trigger DIC?

A

Spesis, shock, trauma → Tissue damage and inflammation lead to an increase in concentration of tissue factor

80
Q

What is tissue factor?

A

Activation of coagulation and stimulates thrombin production

81
Q

How does DIC affect physiology?

A
  1. Compensatory mechanisms may be unable with factor activation
  2. Increased thrombin enhances platelet aggregation
  3. Systematic activation of coagulation pathways also results in an inability to remove fibrin
82
Q

What are the clinical manifestations of DIC?

A
  1. Organ dysfunction
  2. Patients at risk for DVT and PE
83
Q

What do you monitor in patients with DIC?

A
  1. Hematuria (blood in urine)
  2. Hematemesis (blood vomit)
  3. Overt hemorrhage
84
Q

How do you diagnose DIC?

A
  1. Low platelet and fibrinogen levels
  2. Prolongation of PT and aPTT results, with elevation in D-dimer values
85
Q

What is thrombocythemia?

A
  1. Increase platelet > 600,000

Essential thrombocythemia

86
Q

What are the causes of thrombocythemia?

A

Infection or increased inflammation and activation of immune system → overwhelming vWF

87
Q

Clinical manifestations of thrombocythemia?

A
  1. hemmorrhage
  2. Life threatening
  3. HA and visual disturbances
88
Q

Treatment of thrombocythemia?

A
  1. Biologic agents to reduce platelets
  2. Plasmapheresis (plasma exchange)
  3. Low doses of anticoagulants
89
Q
A

Drug Action I (32 decks)

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