Hematology & Immunology Part 1 Flashcards by Carol Dumond

Layer of blood vessel that has endothelial cells that repel blood components from the vessel wall.

Intima

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Layer of blood vessel that is thrombogenic and active

Media

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Layer of blood vessel that controls blood flow by degree of contraction

Externa

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Immediately, the vessel wall contracts to tamponade the area (dec blood flow). This occurs due to the ANS reflexes (expression of TXA2 and ADP)
-Area around injury vasodilates to distribute blood to the surrounding tissues

Vessel Injury

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3 components:
-Adhesion
-Activation
-Aggregation

Formation of the Primary Plug

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vWF emerges from the endothelial cell lining. It is sticky and makes platelets adhere.
-Gp1b is on the surface of platelets and attracts them to the endothelial lining.

Adhesion

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Platelets undergo confirmational changes via Tissue Factor (Extrinsic Clotting Pathway)

Activation

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Platelets form a mound to seal injury

Aggregation

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The activation of cofactors (enzymes) in hemostasis.

Coagulation Cascade

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Contact Activation Pathway; occurs due to injury to blood vessels.

Intrinsic Pathway

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Occurs due to trauma, Tissue Factor
-Injury is outside the vessel wall

Extrinsic Pathway

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Forms the platelet plug; Factor X has been activated by both pathways

Common Pathway

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Requires:
-The conversion of prothrombin to thrombin
-Coagulation proteins from the Liver
-Ca from the diet (positions factors on the surface of the plt so clotting will ensue)
-vWF (synthesized in endothelial cells)
-Factors 2,7,9,10 (dependent on Vit. K)

Coagulation Cascade

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Theory that platelets and the intrinsic/extrinsic pathways are distinct and work interdependently. Explains why certain deficiencies fail to cause bleeding, even w/abnormal lab values.
-Initiation
-Amplification
-Propagation

Cell-Based Theory of Coagulation

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Triggered by injury to the endothelial surface. Tissue Factor recruits plts and activates Factor 7.
-TF/FVII activates Factor X (common pathway) and Factor IX (intrinsic)

Initiation

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Thrombin generation & Activation of clotting factors.
-vWF and Gp1b promote plt aggregation

Amplification

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Activated prothrombin into thrombin, fibrinogen into fibrin. Forms the hemostatic plug - all factors actively influence each other

Propagation

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Hold ASA ____ days prior to surgery

7-10 days

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Hold NSAIDs _____ hours before surgery

24-48 hrs

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Early Pharmacologic treatment for Jehovah’s Witnesses

Erythropoietin and iron

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Dietary: Vitamin K & E, coenzyme Q10, zinc, omega-3 fatty acids

Herbal: garlic, ginger, ginkgo, feverfew, fish oil, flaxseed oil, black cohosh, cranberry

Dietary/Herbals that influence coagulation

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-Measures plt fxn (microvascular contraction): adhesion & aggregation
-Modest prolongation does not predict surgical bleeding; altered by ASA & NSAIDS, Not routine, technician dependent
-Normal 3-7 minutes

Bleeding Time

Actual # of plts in blood/mm^3
Normal count does not imply normal function → fxn maintains vascular integrity, aggregate when plug is necessary to stop bleeding, help initial clotting pathways
-Thrombocytopenia: < 100,000
-Surgical Risk: < 50,000
-Spontaneous bleeding: < 20,000

Platelet Count (normal is 150-300,000)

Evaluates ability to generate enough thrombin to form fibrin to create a stable clot →use this to monitor oral anticoagulant therapy (not sensitive)
-Prolonged with extrinsic pathway & common pathway disorders
-Fails to identify specific defect - but identifies an existing problem
-Altered by coumarin derivatives (warfarin)

Prothrombin Time (PT- normal is 12-14 seconds)

Reported with PT (extrinsic & common pathway)

International Normalized Ratio (INR- 0.8-1.2)

-Prolonged with intrinsic pathway & common pathway disorders -Altered by heparin & LMWH

Activated Partial Thromboplastin Time (aPTT - normal is 25-32 sec)

-Simple, quick → used in surgery to monitor coagulation status -Regulates Heparin Therapy in OR -> 400 seconds for cardiac surgery

Activating Clotting Time (ACT - normal is 90-150 sec)

Measures process of clot formation over time → evaluates plt rxns, coagulation, & fibrinolysis -Machine measures the speed at which a clot forms. Results provide an indication of 1) clot strength 2) platelet number and function 3) intrinsic pathway defects 4) thrombin formation and 5) rate of fibrinolysis

Thromboelastogram (TEG)

Part of TEG; reflects the acceleration of fibrin build-up and cross linking

Alpha Angle

Part of TEG; reflects rxn time and coagulation factor levels

Clotting Time

Part of TEG; reflects stability of the clot

Max Amplitude

-Plan to avoid risks associated w/ transfusion (humor error, infection), know blood product inventory (resources, age of blood), cost-control -Avoid undesirable effects (left shift-decreased 2,3-DPG), coagulopathy, hypothermia, hyperkalemia, acid-base changes, citrate intoxication

Blood Transfusion

Transfusion to improve tissue oxygenation (O2 carrying capacity decreases w/ length of storage) -Not recommended to give for volume expansion

PRBCs

Balance between global O2 delivery (DO2) & O2 consumption (VO2) → O2 extraction ratio (normal 20-30%): DO2 independency (despite anemia, O2 consumption unaffected) -Critical DO2 = DO2 decreases to VO2 → tissue ischemia -DO2 = CO x CaO2 (arterial O2 content) → increase in Hgb increases DO2 but not necessarily VO2/prevents ischemia bc banked blood has depleted 2,3-DPG & decreased capillary fxn

Tissue Oxygenation

What is the 10-30 rule?

Hgb of 10 = Hct of 30%

-Must be ABO compatible -1 unit inc Hgb by 1 g/dL and Hct by 3% Indications: -symptomatic anemia (can be as low as Hgb of 8 unless hypotension/tachycardia occur) massive hemorrhage, decreased O2-carrying capacity

PRBCs

Hgb < 6: transfuse Hgb 6-7: likely indicated to transfuse Hgb 7-8: maybe appropriate if ortho or cardiac surgery; those with stable cardiac disease Hgb 8-10: Not likely indicated unless exceptional circumstances (ongoing bleeding, hem/onc patient, etc).

PRBCs transfusion triggers

Essential to thrombogenesis (contains plt & clotting factors) -Round, disc-like, circulate freely within the blood, formed in the bone marrow, survive 7-10 days; donated plt lifespan = 4-5 days -Flow along the vessel surface (inactive) strategically positioned to react in event of vessel injury → activated in response to vascular trauma, work in conjunction with plasma proteins to build a stable clot

Platelets

-1 unit inc 5-10K (usually given in 6 pack - inc 30-60,000) -Preferred ABO compatible, but not required -Risk of bacterial infection bc stored at room temp (!) Indications: -Thrombocytopenia -Massive hemorrhage, plt function deficit (use TEG) -Likelihood of bleeding (vascular procedures), hazard if bleeding were to occur (Intracranial pressure), and the possibility of additional coagulation disturbance

Platelets

Active bleeding with bleeding time 2x normal Active bleeding with platelet count < 20,000 (non-surgical pts) Active bleeding with platelet count < 50-60,000 (surgical pts) Active bleeding following complete heparin neutralization (post-ECC bypass)

Platelets Transfusion Triggers

-Fluid portion of whole blood (frozen to preserve coagulation factors, thawed on use) -1 unit (250 mL) → 10-15 ml/kg improves clotting to 20-30% of norm -Must be ABO compatible -PT/aPTT > 1.5x normal -Contains: all coagulation factors, proteins C&S, antithrombin 3 -Not indicated if PT or INR and aPTT are normal, or solely for augmentation of plasma volume or albumin concentration

FFP

Indications: -Correction of multiple coagulation deficits -Bleeding from warfarin therapy (INR >2) or reversal of Warfarin tx -Antithrombin 3 deficiency -Massive transfusion/coagulopathy (PRBC 1:FFP 1:Plt 1) -Microvascular bleeding with abnormal coags (coagulation factor deficiency)

FFP

-Obtained by thawing FFP and consolidating the white precipitate by centrifuge → concentrated version of FFP -1 “pool” increases fibrinogen 45 mg/dl -Preferred ABO compatible, but not required -Contains: fibrinogen, factors 5, 8, 13 & vWF

Cryoprecipitate

Indications: -hypofibrinogenemia, massive hemorrhage, bleeding pts w/ vWF unresponsive to desmopressin, fibrinogen < 80-100 mg/dl (w/excessive bleeding) Transfusion Trigger: Transfuse when Fibrinogen <80-100 (or lower if actively bleeding)

Cryo

Universal Recipient

Universal Donor

Type A can receive what blood products?

Type O and Type A

Done within 45 minutes; tells you blood type, Rh factor (risk for autoimmune rxn against own cells), antibody screen for common antibodies

Type and Screen

Does T&S, but then blood units are crossmatched/tagged for the patient and set aside. -If patient has had several transfusions, will take longer to get a crossmatched unit

Crossmatch

Can Rh+ receive Rh- blood?

Yes

Decreased alloimmunization, prevent febrile rxns, reduce CMV transmission, reduced inflammatory mediator accumulation in storage

Leukoreduction

-Patients shift left on OxyHgb curve (decreased 2,3 DPG). Oxygen is not released to tissues. -Coagulopathy -Hypothermia -Hyperkalemia risk if more than 1 unit and patient is unable to excrete K+ -Acid-base Imbalances: Banked blood is acidotic -Citrate intoxication: can cause ionized hypocalcemia (especially in patients in Liver failure who are unable to get rid of citrate).

PRBC side effects

When the risks of decreased O2 carrying capacity exceeds risks of transfusion, clinical judgment based on patient issues, types of surgery, ongoing blood loss, evaluate transfusion w/ indicators of peripheral tissue oxygenation

PRBCs transfusion trigger

Parasites, viral (hepatitis, HIV, HTLV, CMV, West Nile Virus), prions (CJD-mad cow), bacterial (more common)

Infection risk of transfusion