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Pharm Final review > Principles hematology > Flashcards

Principles hematology Flashcards

1
Q

Three layers of the vessel wall

A

Intima: Inner, primarily endothelial cells

Media: middle subendothelial, contains collagen and bibronectin

Adventitia: outer, Controls blood flow by influencing the vessel’s degree of contraction

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2
Q

Procoagulants

A

Coagulation factors, collagen, vWF, protein C, protein S, fibronectin, thrombomodulin

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3
Q

Anticoagulant

A

antithrombin III

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4
Q

Vasodilation

A

nitric oxide
prostacyclin

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5
Q

vasoconstriction

A

thromboxane A2
ADP
serotonin

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6
Q

fibrinolytic

A

plasminogen
tPA
urokinase

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7
Q

antifibrinolytic

A

plasminogen activator inhibitor

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8
Q

Stages of vessel injury

A

The vessel wall immediately contracts to cause a tamponade, thereby decreasing blood flow

The area adjacent to the injury vasodilates and distributes blood to the surrounding organs and tissues

Contraction is followed by three separate stages in the formation of a primary plug:
1. adhesion (vWF)
2. activation
3. aggregation

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9
Q

What are the two separate pathways of the clotting cascade?

A

extrinsic and intrinsic

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10
Q

Extrinsic (tissue factor) pathway

A

Activated by release of tissue factor (TF) when damage occurs outside the vessel wall (i.e., organ trauma, crushing injury)

TF (factor III) activates proconvertin (factor VII) changing it to activated factor VII (VIIa)
Once activated, factor VII activates factor X (Stuart-Prower) of the common pathway
Factor X forms a complex with factor V (proaccelerin, a prothrombinase complex), activating factor II (prothrombin), which when activated becomes factor IIa (prothrombin)
Thrombin then activates factor I (fibrinogen) to form activated factor I (Ia, fibrin)

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11
Q

Clotting pathway

A
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12
Q

Intrinsic pathway (Contact activation pathway)

A

Initiated when damage occurs to the blood vessels themselves

Initiated by prekallikrein, high-molecular-weight kininogen (HMWK) , and by the activation of XII (Hageman)

With the help of calcium (factor IV), the coagulation pathways initiates a domino effect

Once activated, each factor activates its subsequent factor.

Factor XII activates factor XI, which activates factor IX, which then activates factor VIII, and ultimately merges at the common pathway and activates factor X. The result is the generation of fibrin from the activation of prothrombin to thrombin.

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13
Q

What factors does thrombin assist with?

A

activating factors V, VIII, I, and XIII

Influences platelet recruitment to the site of injury

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14
Q

Common Pathway

A

The terminal pathway of the coagulation cascade

Factor X has been activated by the extrinsic and intrinsic pathways

Factor X requires factor V (proaccelerin) and calcium to convert factor II (prothrombin) to its active-state thrombin (IIa)

Thrombin then activates factor I (fibrinogen)to its active form Ia (fibrin)

Factor XIII (fibrin-stabilizing factor) is required for the platelet plug to hold. It forms a cross-linked mesh within the platelet plug, increasing its strength.

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

Once a clot is made, it retracts, eliminating its serum

As the clot retracts, it weaves the edges of the vessel together, healing the injury

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15
Q

All the clotting factors and their names

A
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16
Q

What is fibrinolysis regulated by?

A

Fibrinolysis is regulated by plasma proteins

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17
Q

What does the Fibrinolytic System do?

A

Degrades fibrin once the hemostatic plug is no longer needed

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

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18
Q

Which pathway do PT and aPTT go with?

A

PT - extrinsic

aPTT - intrinsic

normal PT 12-14 seconds
normal PTT 25-32 seconds
normal ACT 50-150

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19
Q

Platelet Infusion Guidelines

A

**Recommended dose: 1 plateletpheresis pack per 10 kg of body weight. This dose should increase the platelet count by 5,000 to 10,000 mm

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

Normal lifespan: 7 to 10 days
Donated platelet lifespan: 4 to 5 days

20
Q

Fresh Frozen Plasma Infusion Guidelines

A

*Contains all the clotting factors and naturally occurring inhibitors

Does not provide platelet replacement

Must be ABO compatible

Average FFP volume: 200 to 250 mL

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 patients transfused with more than one blood volume (approximately 70 mL/kg) and when PT/INR and an APTT cannot be obtained

Urgent reversal of warfarin therapy when prothrombin complex concentrate (PCC) is not available

Correction of a known coagulation factor deficiency for which specific concentrates are unavailable

FFP NOT indicated for:
PT/INR and APTT normal
Solely for increasing albumin level or plasma volume

21
Q

Cryoprecipitate Infusion Guidelines

A

The precipitate collected off the top of FFP as it thaws

Rich in factors VIII, XIII, and fibronectin

Fibrinogen concentration < 80 to 100 mg/dL in the presence of bleeding

An adjunct in massively transfused patients where a fibrinogen level is not obtainable

Patients with congenital fibrinogen deficiencies

Rarely indicated if fibrinogen concentration is > 150 mg/dL

22
Q

Transfusion Guidelines

A

Few fixed guidelines for transfusion

Guidelines vary by institution

Hgb < 7g/dL is recommended for high-risk patients

Alternatives to PRBC transfusion:
- Preoperative autologous donation
- Acute normovolemic hemodilution
- Blood cell salvage
- 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

23
Q

How much does 1 unit of prbc’s (350ml) increase hemoglobin by?

A

by 1g/dL

24
Q

How much does 1 unit of platelets (250 ml) increase platelets by?

A

30,000-60,000

25
Q

Von Willebrand Disease (vWD):

A

Rare bleeding disorder

Can be inherited or acquired (secondary to cardiovascular, malignant, or immunologic diseases)

26
Q

Von Willebrands treatment options

A

Desmopressin, high-dose IV immunoglobulins, FVIII/vWF concentrates, plasma exchange

Type 1: desmopressin
Type 2 and 3: require vWF concentrate administration

Tranexamic acid is also an important adjunctive therapy as either

27
Q

Hemophilia A is a Factor _____ deficiency
Hemophilia B is a Factor _____ deficiency

A

Hemophilia A: Factor VIII deficiency

Hemophilia B: Factor IX deficiency

28
Q

Hemophilia symptoms

A

Spontaneous bleeding
Muscle hematomas
Joint pain

29
Q

Treatment for hemophilia

A

Desmopressin
Factor VII

30
Q

Perioperative Management of the Hemophilic Patient:

A

Preoperative assessment of inhibitor screening and inhibitor assay completed within 1 week of surgery

Elective procedures early in the day

Desmopressin is ok for hemophilia A but of no use in hemophilia B because it does not affect factor 9. Cryo preferred over ffp for A

Treatment with viral inactivated plasma-derived or recombinent concentrates is preferred over cryo or ffp.

31
Q

Disseminated Intravascular Coagulation (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

Systemic coagulation activation results in intravascular fibrin deposits, thrombotic microangiography, compromised blood supply to organs, and multiorgan system failure

32
Q

DIC diagnosis

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 affitmative of nonovert DIC)

33
Q

Treatment of DIC

A

Depends on the underlying condition

Identify and eliminate the underlying cause

No treatment if mild, asymptomatic, and self-limited

Obstetrics: DIC many resolve with prompt delivery of the fetus

Sepsis: antibiotics

Platelets, FFP, cryoprecipitate

Antithrombotics are controversial

34
Q

Sickle Cell Disease

A

Common, hereditary hemoglobinopathy

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

Hemoglobin SS
Hemoglobin SC
Hemoglobin SB- (Beta) thalassemia
Beta-zero thalassemia

35
Q

Sickle Cell Disease: Intraoperative Management

A

Adequate hydration

avoid hypoxemia

maintain normothermia

they have LOTS OF PAIN

caution using vasoocclusive devices like tournaquets

for patients with pulmonary disease, maybe decrease hemoglobin S level to below 30%

36
Q

Heparin-Induced Thrombocytopenia (HIT):

A

An immune response to heparin that can progress to severe thrombosis, amputation, and death
Suspect HIT when a patient receiving heparin experiences a 50%+ drop in platelet count

37
Q

Clinical presentation of HIT

A

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

38
Q

Gold standard DIAGNOSIS OF hit

A

C-serotonin release assay

39
Q

Treatment of HITBased on clinical presentation and laboratory findings

Stop heparin immediately

Administer direct thrombin inhibitors (argatroban or lepirudin)

Prompt surgical intervention for thrombosis that compromises peripheral perfusion

A
40
Q

Type 1 HIT vs Type 2 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

41
Q

Type 1 HIT vs 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

42
Q

Differences type 1 and type 2 HIT

A

Type 2 takes longer to develop, is worse, is immune mediated, severe thrombocytopenia, and occur with any dose or route

43
Q

slide 33

A

slide 33

44
Q

Additional Risk Factors for Acute coronary 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

45
Q

Patient risk factors for coronary stents

A

Patient Risk Factors:
Advanced age
Diabetes mellitus
Gene polymorphism
Hypercoagulable states (e.g., diabetes, malignancy, and surgery)
Major cardiac adverse event within 30 days of percutaneous cardiac intervention
Reduced left ventricular ejection fraction
Prior brachytherapy
Renal insufficiency

46
Q

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

A

Elective noncardiac surgery should be delayed 30 days after bare metal stent placement and 6 months after drug eluting stent placement

Pharm Final review (24 decks)

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