Hematology & Immunology Part 1 Flashcards

1
Q

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

A

Intima

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2
Q

Layer of blood vessel that is thrombogenic and active

A

Media

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3
Q

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

A

Externa

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4
Q

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

A

Vessel Injury

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5
Q

3 components:
-Adhesion
-Activation
-Aggregation

A

Formation of the Primary Plug

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6
Q

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.

A

Adhesion

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7
Q

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

A

Activation

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8
Q

Platelets form a mound to seal injury

A

Aggregation

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9
Q

The activation of cofactors (enzymes) in hemostasis.

A

Coagulation Cascade

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10
Q

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

A

Intrinsic Pathway

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11
Q

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

A

Extrinsic Pathway

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12
Q

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

A

Common Pathway

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13
Q

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)

A

Coagulation Cascade

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14
Q

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

A

Cell-Based Theory of Coagulation

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15
Q

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)

A

Initiation

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16
Q

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

A

Amplification

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17
Q

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

A

Propagation

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18
Q

Hold ASA ____ days prior to surgery

A

7-10 days

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19
Q

Hold NSAIDs _____ hours before surgery

A

24-48 hrs

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20
Q

Early Pharmacologic treatment for Jehovah’s Witnesses

A

Erythropoietin and iron

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21
Q

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

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

A

Dietary/Herbals that influence coagulation

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22
Q

-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

A

Bleeding Time

23
Q

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

A

Platelet Count (normal is 150-300,000)

24
Q

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)

A

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

25
Q

Reported with PT (extrinsic & common pathway)

A

International Normalized Ratio (INR- 0.8-1.2)

26
Q

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

A

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

27
Q

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

A

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

28
Q

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

A

Thromboelastogram (TEG)

29
Q

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

A

Alpha Angle

30
Q

Part of TEG; reflects rxn time and coagulation factor levels

A

Clotting Time

31
Q

Part of TEG; reflects stability of the clot

A

Max Amplitude

32
Q

-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

A

Blood Transfusion

33
Q

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

A

PRBCs

34
Q

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

A

Tissue Oxygenation

35
Q

What is the 10-30 rule?

A

Hgb of 10 = Hct of 30%

36
Q

-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

A

PRBCs

37
Q

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).

A

PRBCs transfusion triggers

38
Q

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

A

Platelets

39
Q

-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

A

Platelets

40
Q

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)

A

Platelets Transfusion Triggers

41
Q

-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

A

FFP

42
Q

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)

A

FFP

43
Q

-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

A

Cryoprecipitate

44
Q

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)

A

Cryo

45
Q

Universal Recipient

A

AB

46
Q

Universal Donor

A

O

47
Q

Type A can receive what blood products?

A

Type O and Type A

48
Q

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

A

Type and Screen

49
Q

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

A

Crossmatch

50
Q

Can Rh+ receive Rh- blood?

A

Yes

51
Q

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

A

Leukoreduction

52
Q

-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).

A

PRBC side effects

53
Q

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

A

PRBCs transfusion trigger

54
Q

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

A

Infection risk of transfusion