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Principles-Other > Hematology > Flashcards

Hematology Flashcards

1
Q

What are the 3 layers of the blood vessel?

A

Inner
media
adventitia

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2
Q

What does the inner layer (intima) do?

A

Separates flowing blood from the vessel

Made primarily of endothelial cells which play an important role in homeostasis by synthesizing and secreting procoagulants, anticoagulants, and fibrinolytics

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3
Q

What substances does the intima synthesize and secrete?

A

Von Willebrand Factor (vWF)

Tissue Factor

Thromboxane A2

Adenosine diphosphate (ADP)

Nitric oxide (NO)

Prostacyclin

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4
Q

What is the media layer?

A

Sub endothelial layer

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5
Q

What does the media contain?

A

Collagen

Fibronectin

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6
Q

What does the adventitia do?

A

controls blood flow by influencing the vessel’s degree of contraction

(NO and prostacyclin work here)

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7
Q

What is Von Willebrand factor (vWF) do?

A

Platelet adhesion

a necessary cofactor for adherence of platelets to the subendothelial layer

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8
Q

What does Tissue Factor (TF) do?

A

A cofactor from the coagulation cascade

Activates the clotting cascade pathway when injury to a vessel occurs

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9
Q

What does Thromboxane and adenosine diphosphate (ADP) do?

A

vascular smooth muscle constriction

controls blood flow by influencing vasoconstriction

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10
Q

What does nitric oxide (NO) and prostacyclin do?

A

Vascular smooth muscle relaxation

control blood flow by vasodilation of blood vessels

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11
Q

What does collagen do?

A

a potent stimulus for platelet attachment to an injured vessel wall

Tensile strength

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12
Q

What does fibronectin do?

A

facilitates the anchoring of fibrin during the formation of a hemostatic plug

cell adhesion

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13
Q

What are the procoagulants?

A

Coagulation factors

Collagen

vWF

Fibronectin

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14
Q

What are the anticoagulants?

A

Protein C

Protein S

Antithrombin

Tissue pathway factor inhibitor

Thrombomodulin

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15
Q

What are the fibrinolytics?

A

Plasminogen

tPA

Urokinase

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16
Q

What are the antifibrinolytics?

A

Alpha-antiplasmin

Plasminogen activator inhibitor

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17
Q

What are the vasoactive mediators

A

vasoconstrictors: Thromboxane A2, ADP, serotonin

vasodilators: nitric oxide, prostacyclins

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18
Q

What does antithrombin III

A

anticoagulant: degrades factors XII, XI, IX, and II

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19
Q

What are the 4 steps of hemostasis?

A

1.) vascular spasm

2.) formation of platelet plug (primary homeostasis)

3.) coagulation and fibrin formation (secondary homeostasis)

4.) fibrinolysis when clot is no longer needed

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20
Q

What are the 3 steps in the formation of the primary plug?

A

Adhesion
Activation
Aggregation

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21
Q

What happens during adhesion?

A
  • vWF mobilizes from within the endothelial cells and emerges from the endothelial lining

-glycoprotein 1b (Gp1b) receptors emerge from the surface of the platelet

-Gp1b attaches to vWF and attracts platelets to the endothelial lining

-vWF makes platelets “sticky” and allows them to adhere to the site of injury

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22
Q

What happens during activation?

A
  • Under the influence of tissue factor (TF), the platelet undergoes a conformational change as it becomes activated

-The once disk-like structure swells and becomes oval and irregular

-Glycoproteins IIb and IIIa project outward from the platelet surface

-the Gp11b and 111a complex links activated platelets together to form a primary platelet plug

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23
Q

What happens during aggregation?

A

-As platelets undergo activation, they release alpha and dense granules, contractile granules, thrombin and many mediators into the blood to promote procoagulant activity

-these mediators are responsible for platelet aggregation to form a primary unstable clot

-with a minor injury this clot is enough to maintain homeostasis

-with a major injury, activation of the coagulation clotting cascade is required for permanent repair

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24
Q

What does thrombin do?

A

Assists in activating factors 1, 5, 8 and 13

influences platelet recruitment to the site of injury

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25
Q

what are thrombin’s anticoagulant actions?

A

-Prevents runaway clot formation by releasing tissue plasminogen activator (tPA) from endothelial cells

-Stimulates protein C and protein S to inhibit clot formation

-forms a relationship w antithrombin III to interfere w coagulation

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26
Q

Factor 10 requires what to convert factor II (prothrombin) to its active state thrombin (IIa)

A

Factor 5 (proaccelerin) and calcium

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27
Q

What does thrombin do?

A

Assists in activating factors
1
5
8
13

influences platelet recruitment to the site of injury

enough thrombin must be present to activate adequate fibrin to form a stable clot

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28
Q

What is the common pathway?

A

the terminal pathway of the coagulation cascade

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29
Q

What factor is required for the platelet plug to hold?

A

Factor XIII (fibrin-stabilizing factor)

if forms a cross-linked mesh within the platelet plug, increasing its strength

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30
Q

What factors secure a stable secondary plug?

A

Fibrin (factor 1a) and factor XIII secure a stable secondary plug and bleeding stops

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31
Q

What is the fibrinolytic system?

A

It degrades fibrin once the hemostatic plug is no longer needed.

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32
Q

How does thrombin work within the fibrinolytic system?

A

Thrombin which originally acted as a procoagulant, now acts as an anticoagulant and activates additional anticoagulant mediators

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33
Q

What factors do protein C and S inhibit in the fibrinolytic system?

A

III, V, VIII
3, 5, 8

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34
Q

What does antithrombin III do?

A

inhibits thrombin activity by sequestering factors
IX- 9
X- 10
XI-11
XII1- 12

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35
Q

what are some prescription or OTC meds that affect coagulation?

A

Anticoagulants (heparin)
Procoagulants (vit K)
antiplatelets (NSAIDs)
Antifibrinolytics (amicar, TXA)
dietary supplements (vit K, E, zinc omega-3 fatty acids)
Herbal supplents (garlic, ginko, ginger, fish oil, feverfew, flaxseed oil, black cohost, cranberry)

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36
Q

How is a plateletpheresis pack dosed?

A

1 pack per 10kg of body wt

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37
Q

How much should a plateletpheresis pack increase the platelet count?

A

5,000 -10,000mm

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38
Q

What carries the greatest risk of bacterial transmission?

A

Platelets d/t storage at room temp for 4-5 days

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39
Q

normal platelet lifespan:

A

7-10 days

40
Q

donated platelet lifespan:

A

4-5daus

41
Q

what are the ASA transfusion taskforce recommendations?

A

Platelet transfusion even with a normal or absent platelet count if there is known or suspected platelet dysfunction

In surgical and obstetric patients, platelet transfusion is rarely indicated if platelet count is > 100,000 μL.

Transfusion is indicated for platelet count < 50,000 μL

Compatible platelets are recommended, but unmatched platelets can be administered if matched platelets are unavailable. However, incompatibility shortens the lifespan of the platelet.

42
Q

What does FFP contain?

A

all the clotting factors and naturally occuring inhibitors

43
Q

Does FFP provide platelet replacement?

A

NO

44
Q

Does FFP have to be ABO compatible?

A

YES

45
Q

What is the average FFP volume?

A

200-250mL

46
Q

What are the indications for FFP?

A

-correction of excessive microvascular bleeding in the presence of an INR >2.0 and the absence of heparin

Correction of excessive microvascular bleeding secondary to coagulation factor deficiency in pts transfused w more than one blood volume (approx 70ml/kg) and when PT/INR and APTT cannot be obtained

urgent reversal of warfarin therapy w prothrombin complex concentrate (PCC) is not available

correction of know coagulation factor deficiency for which specific concentrates are unavailable

47
Q

What is FFP NOT indicated for?

A

PT/INR and APTT normal

solely for increasing albumin level or plasma volume

48
Q

What is cryo?

A

The precipitate collected off the top of FFP as it thaws

49
Q

What is cryo rich in?

A

factors VIII (8), XIII (13), and fibronectin

50
Q

What are the indications for cryo?

A

fibrinogen activity test suggesting fibrinolysis

fibrinogen concentrations <80- 100mg.dL in the presence of bleeding

an adjunct in massively transfused pts where fibrinogen levels are not obtainable

pts w congenital fibrinogen deficiencies

51
Q

When is cryo not indicated?

A

Rarely indicated if fibrinogen concentration is >150 mg/dL

52
Q

What are some alternatives to PRBC transfusion?

A

preop autologous donation
acute normovolemic hemodilution
blood cell salvage
recombinant factor VII

53
Q

What is recombinant factor VII?

A

Used to treat hemophilia A (factor VIII) and B (factor IX), inhibitor disorders of factors VIII and IX, factor VII deficiency, and as a universal hemostatic agent

Use cautiously in patients with a history of thrombosis

54
Q

PRBC:

A

1 unit (350 mL) increase hgb by 1g/dL (10g/L)

use: symptomatic anemia

55
Q

Platelets:

A

1 unit (250mL) increases platelets by 30,000-60,000

use: thrombocytopenia, massive hemorrhage, platelet dysfunction

56
Q

FFP:

A

1 unit (250mL)
contains all coag factors espec. II, VII, IX, X, proteins C &S and antithrombin III

use: bleeding from warfarin, mass transfusion, thrombotic thromboytopenic purpura, antithrombin III deficieincies

57
Q

cryoprecipitate:

A

20mL contains 200 mg fibrinogen, 70-80 units of factor 8

contains: fibrinogen, factor 5, 8, 13 and vWF

Indications: hypofibrinogenemia, mass hemorrhage

58
Q

desmopressin

A

dose: 0.3-0.4 mcg/kg

stimulates release if vWF

use: uremic platelet dys, vWF disease

59
Q

vitamin K:

A

10 mg IM, IV or SQ

stimulates activation of factors 2, 5, 7, and 9, protein c and s

use: liver dys, bleeding from warfarin

60
Q

protamine:

A

1mg neutralizes 100 units of heparin

reversal of heparin therapy

61
Q

factor 7:

A

50mcg/kg

recombinant factor VIIa

use: hemophilia

62
Q

aminocaproic acid:

A

0.1g/kg loading dose, 1g/hr

plasminogen inhibitor

primary fibrinolysis

63
Q

What is von Willebrand disease (vWD)

A

rare bleeding disorder
several subtypes
can be inherited or acquired (secondary to CV, malignant or immunologic disease)

64
Q

What are the lab findings for vWD?

A

prolonged bleeding time

vWF deficiency

factor 8

decreased vWF activity as measured by ristocetin cofactor assay (RCoF)

decreased factor VIII coagulant activity (VIII:C)

65
Q

What are the signs and symptoms of vWD?

A

inherited: lifelong bleeding episodes

acquired: sudden onset of bleeding symptoms

66
Q

treatment for vWD

A

desmopressin

high-dose IV immunoglobulins

FVIII/vWF concentrates

plasma exchange

67
Q

What is hemophilia?

A

X-linked recessive disorder characterized by unpredictable bleeding

-females carry the gene
-only affects males

68
Q

Hemophilia A:

A

Factor VIII deficiency (8)

69
Q

Hemophilia B:

A

Factor IX deficiency (9)

70
Q

symptoms of hemophilia

A

spontaneous bleeding
muscle hematomas
joint pain

71
Q

treatment for hemophilia:

A

desmopressin
factor VII

72
Q

preop assessement for hemophilia

A

Pt, aPTT, factor 8, factor 9, fibrinogen

type and crossmatch

73
Q

What is DIC?

A

A result of intravascular coagulation activation with microvascular thrombi formation, which causes thrombocytopenia and clotting factors depletion, leading to bleeding and end-organ complications

Coagulation activation ranges from mild thrombocytopenia and prolonged clotting times to acute DIC characterized by extensive bleeding and thrombosis

74
Q

What is acute DIC?

A

manifests as complications from multiple diseases (sepsis, post-op, ob complications, blood transfusion reactions and certain malignancies such as acute promyelocytic leukemia)

75
Q

What is chronic DIC

A

seen in solid tumors and large aortic aneurysms

76
Q

what is the clinical presentation of DIC?

A

acute (overt) dic: ecchymosis, petechiae, mucosal bleeding, depletion of platelets and clotting factors, and bleeding at puncture sites

chronic (nonovert) DIC: thromboembolism, and evidence of coagulation system activation

77
Q

What’s the diagnosis for DIC?

A

Laboratory tests: platelet count, aPTT, PT, fibrin-related markers (fibrin degradation products, D-dimer), fibrinogen, and antithrombin

International Society of Thrombosis and Hemostasis (ISTH) developed a DIC scoring system (score > 5 overt DIC, < 5 suggestive but not affirmative of nonovert DIC)

78
Q

What is the treatment o DIC?

A

Dependent on underlying cause

OB: DIC may resolve within prompt delivery of fetus

sepsis: antibiotics

platelets, FFP, cry

antithrombotics are controversial

79
Q

What is sickle cell disease?

A

common hereditary hemoglobinopathy

an autosomal recessive genetic abnormality of the beta-globin that codes for production of variant hemoglobin, hemoglobin S

80
Q

what are the types of sickle cell disease?

A

-hemoglobin SS
hemoglobin SC
Hemoglobin S(beta) thalassemia
beta-zero thalassemia

81
Q

What is HIT?

A

Immune response to heparin that can progress to severe thrombosis, amputation and death

82
Q

When should HIT be suspected?

A

when a pt receiving heparin experiences a 50% + drop in platelet count

83
Q

What is the clinical presentation of HIT?

A

thrombocytopenia
resistance to heparin anticoagulation
thrombosis
positive assay tests indicative of HIT

2 types:
type 1
Type 2

84
Q

How do you diagnose HIT?

A

gold standard: c-serotonin assay

other tests: heparin-induced platelet aggregation assay, and antibody detection via enzyme-linked immunosorbent assay

85
Q

Whats the treatment for HIT?

A

based on clinical and lab findings

stop heparin immediately

administer direct thrombin inhibitors (argatroban or lepirudin)

prompt surgical intervention for thrombosis that compromises peripheral perfusion

86
Q

Type 1 HIT:

A

Type I:
* Thrombocytopenia is mediated by direct heparin-induced platelet
aggregation (e.g., nonimmune mediated)

Onset is typically 1 to 4 days after start of heparin therapy

  • Mild thrombocytopenia (e.g., less than 100,000 per microliter)
  • Thrombocytopenia often resolves spontaneously even with
    continued administration of heparin
  • Typically occurs with high-dose heparin administration
  • Not associated with thrombosis and serious clinical sequelae
87
Q

Type 2 HIT:

A

Type II:
* Thrombocytopenia is mediated by the actions of the heparin,
platelet factor 4, and immunoglobulin G expression (e.g.,
immune-mediated)

  • Onset is typically 5 to 14 days after start of heparin therapy
  • Severe thrombocytopenia (e.g., less than 60,000 per microliter)
  • Thrombocytopenia does not resolve spontaneously, therefore
    heparin administration must be discontinued
  • Occurs with any heparin dose and route
  • Associated with thrombosis and serious clinical sequelae
88
Q

arachidonic acid inhibitors:

A

COX Inhibitors: aspirin, indobufen, triflusal, nonsteroidal, anti-inflammatory agents, sulfinpyrazone

Non-COX inhibition of arachidonic acid; phosphodiesterase inhibitors: dipyridamole, pentoxifylline, cilostazol, trapidil

Other: omega-3 fatty acids, eicosanoids (prostacyclin, prostaglandin analogues)

89
Q

PzY12 ADP receptor inhibitors:

A

Thienopyridines (ADP antagonists): ticlopidine, clopidogrel, prasugrel

ATP derivatives: cangrelor

CPTPs: ticagrelor

90
Q

Thrombin protease-activated receptor -1 inhibitors:

A

ticagrelor

91
Q

Platelet glycoprotein IIB/IIIa receptor blockers:

A

Intravenous: abciximab, tirofiban, eptifibatide

92
Q

drugs w secondary antiplatelet activity

A

Direct thrombin inhibitors, heparin, nitrates, fibrates, calcium channel antagonists, others

93
Q

Anticoagulants:

A

LMWH
Heparin
Fondaparinux
Warfarin
Apixaban
Dabigatran

94
Q

fibrinolytics:

A

t-PA
Streptokinase

95
Q

risk factors for acute stent thrombosis

A

-Site of stent placement (e.g., bifurcation stenting, side branch occlusion)
-Left main coronary artery stent
-Long stent length (greater than 18 mm)
-Ostial stenting
-Overlapping stents
-Placement of multiple stents
-Small stent diameter (less than 3 mm)
-Suboptimal stent placement

96
Q

Elective noncardiac surgery should be delayed ______ days after bare metal stent placement and _______ months after drug-eluting stent placement

A

30 days after bare metal stent
6 months after drug-eluting stent

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