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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
what are thrombin's anticoagulant actions?
-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
26
Factor 10 requires what to convert factor II (prothrombin) to its active state thrombin (IIa)
Factor 5 (proaccelerin) and calcium
27
What does thrombin do?
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
28
What is the common pathway?
the terminal pathway of the coagulation cascade
29
What factor is required for the platelet plug to hold?
Factor XIII (fibrin-stabilizing factor) if forms a cross-linked mesh within the platelet plug, increasing its strength
30
What factors secure a stable secondary plug?
Fibrin (factor 1a) and factor XIII secure a stable secondary plug and bleeding stops
31
What is the fibrinolytic system?
It degrades fibrin once the hemostatic plug is no longer needed.
32
How does thrombin work within the fibrinolytic system?
Thrombin which originally acted as a procoagulant, now acts as an anticoagulant and activates additional anticoagulant mediators
33
What factors do protein C and S inhibit in the fibrinolytic system?
III, V, VIII 3, 5, 8
34
What does antithrombin III do?
inhibits thrombin activity by sequestering factors IX- 9 X- 10 XI-11 XII1- 12
35
what are some prescription or OTC meds that affect coagulation?
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)
36
How is a plateletpheresis pack dosed?
1 pack per 10kg of body wt
37
How much should a plateletpheresis pack increase the platelet count?
5,000 -10,000mm
38
What carries the greatest risk of bacterial transmission?
Platelets d/t storage at room temp for 4-5 days
39
normal platelet lifespan:
7-10 days
40
donated platelet lifespan:
4-5daus
41
what are the ASA transfusion taskforce recommendations?
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
What does FFP contain?
all the clotting factors and naturally occuring inhibitors
43
Does FFP provide platelet replacement?
NO
44
Does FFP have to be ABO compatible?
YES
45
What is the average FFP volume?
200-250mL
46
What are the indications for FFP?
-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
What is FFP NOT indicated for?
PT/INR and APTT normal solely for increasing albumin level or plasma volume
48
What is cryo?
The precipitate collected off the top of FFP as it thaws
49
What is cryo rich in?
factors VIII (8), XIII (13), and fibronectin
50
What are the indications for cryo?
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
When is cryo not indicated?
Rarely indicated if fibrinogen concentration is >150 mg/dL
52
What are some alternatives to PRBC transfusion?
preop autologous donation acute normovolemic hemodilution blood cell salvage recombinant factor VII
53
What is recombinant factor VII?
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
PRBC:
1 unit (350 mL) increase hgb by 1g/dL (10g/L) use: symptomatic anemia
55
Platelets:
1 unit (250mL) increases platelets by 30,000-60,000 use: thrombocytopenia, massive hemorrhage, platelet dysfunction
56
FFP:
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
cryoprecipitate:
20mL contains 200 mg fibrinogen, 70-80 units of factor 8 contains: fibrinogen, factor 5, 8, 13 and vWF Indications: hypofibrinogenemia, mass hemorrhage
58
desmopressin
dose: 0.3-0.4 mcg/kg stimulates release if vWF use: uremic platelet dys, vWF disease
59
vitamin K:
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
protamine:
1mg neutralizes 100 units of heparin reversal of heparin therapy
61
factor 7:
50mcg/kg recombinant factor VIIa use: hemophilia
62
aminocaproic acid:
0.1g/kg loading dose, 1g/hr plasminogen inhibitor primary fibrinolysis
63
What is von Willebrand disease (vWD)
rare bleeding disorder several subtypes can be inherited or acquired (secondary to CV, malignant or immunologic disease)
64
What are the lab findings for vWD?
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
What are the signs and symptoms of vWD?
inherited: lifelong bleeding episodes acquired: sudden onset of bleeding symptoms
66
treatment for vWD
desmopressin high-dose IV immunoglobulins FVIII/vWF concentrates plasma exchange
67
What is hemophilia?
X-linked recessive disorder characterized by unpredictable bleeding -females carry the gene -only affects males
68
Hemophilia A:
Factor VIII deficiency (8)
69
Hemophilia B:
Factor IX deficiency (9)
70
symptoms of hemophilia
spontaneous bleeding muscle hematomas joint pain
71
treatment for hemophilia:
desmopressin factor VII
72
preop assessement for hemophilia
Pt, aPTT, factor 8, factor 9, fibrinogen type and crossmatch
73
What is DIC?
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
What is acute DIC?
manifests as complications from multiple diseases (sepsis, post-op, ob complications, blood transfusion reactions and certain malignancies such as acute promyelocytic leukemia)
75
What is chronic DIC
seen in solid tumors and large aortic aneurysms
76
what is the clinical presentation of DIC?
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
What's the diagnosis for DIC?
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
What is the treatment o DIC?
Dependent on underlying cause OB: DIC may resolve within prompt delivery of fetus sepsis: antibiotics platelets, FFP, cry antithrombotics are controversial
79
What is sickle cell disease?
common hereditary hemoglobinopathy an autosomal recessive genetic abnormality of the beta-globin that codes for production of variant hemoglobin, hemoglobin S
80
what are the types of sickle cell disease?
-hemoglobin SS hemoglobin SC Hemoglobin S(beta) thalassemia beta-zero thalassemia
81
What is HIT?
Immune response to heparin that can progress to severe thrombosis, amputation and death
82
When should HIT be suspected?
when a pt receiving heparin experiences a 50% + drop in platelet count
83
What is the clinical presentation of HIT?
thrombocytopenia resistance to heparin anticoagulation thrombosis positive assay tests indicative of HIT 2 types: type 1 Type 2
84
How do you diagnose HIT?
gold standard: c-serotonin assay other tests: heparin-induced platelet aggregation assay, and antibody detection via enzyme-linked immunosorbent assay
85
Whats the treatment for HIT?
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
Type 1 HIT:
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
Type 2 HIT:
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
arachidonic acid inhibitors:
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
PzY12 ADP receptor inhibitors:
Thienopyridines (ADP antagonists): ticlopidine, clopidogrel, prasugrel ATP derivatives: cangrelor CPTPs: ticagrelor
90
Thrombin protease-activated receptor -1 inhibitors:
ticagrelor
91
Platelet glycoprotein IIB/IIIa receptor blockers:
Intravenous: abciximab, tirofiban, eptifibatide
92
drugs w secondary antiplatelet activity
Direct thrombin inhibitors, heparin, nitrates, fibrates, calcium channel antagonists, others
93
Anticoagulants:
LMWH Heparin Fondaparinux Warfarin Apixaban Dabigatran
94
fibrinolytics:
t-PA Streptokinase
95
risk factors for acute stent thrombosis
-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
Elective noncardiac surgery should be delayed ______ days after bare metal stent placement and _______ months after drug-eluting stent placement
30 days after bare metal stent 6 months after drug-eluting stent

Principles-Other (6 decks)

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