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Flashcards in Hematology Physiology Deck (48):
1

♣ Based on carbohydrate antigens (A and B) present on RBC membrane either as glycoprotein or glycosphingolipids
♣ All individuals produce antibodies to the AB carbohydrate antigen that they lack
♣ Two genes, one on each of two paired chromosomes, determine the O-A-B blood type

Blood Groups

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Why are agglutinins produced in people who do not have the respective agglutinogens in their red blood cells?

Small amounts of these agglutinogens enter through food and bacteria which initiate the production of agglutinins.

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Universal Donor

Blood Type O

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Universal Recipient

Blood Type AB

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♣ Blood group with 6 antigens: C, D, E, c, d, e
♣ Agglutinins are produced after massive exposure to the Rh agglutinogens
♣ Most widely prevalent antigen is D

Rh Blood Group

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If you have the D antigen

Rh+

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If you do not have D antigen or you have the rest of the antigens

Rh-

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Identifying blood type (ABO with Anti-A and Anti-B sera and Rh with anti-D serum)
♣ “Forward” Identify antigen by antisera
♣ “Reverse” Identify isoagglutinin in serum

Pretesting of Blood

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Antigen-antibody complexes causes agglutination ->
Clumps of RBCs pass thru small blood vessels ->
Physical distortion, phagocytic attack in a few days ->

Delayed hemolysis

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Massive amounts of antibodies meet antigenic donor RBCs -> Activate complement and rupture of membranes ->

Immediate hemolysis

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- Increases oxygen-carrying capacity and volume expansion
- Ideal for cases of acute hemorrhage of more than 25% of blood volume

Whole Blood

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- Increase oxygen-carrying capacity
- Should only be given to those with anemia and symptoms
o Dizziness
o Increased heart rate
o Difficulty of breathing

Packed Red Blood Cells

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- Reduces risk of mucosal bleeding

Platelet concentrates

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Thresholds for transfusion of Platelet concentrates

o Patient w/o fever or infection 5,000/uL
o Patient w/ fever of infection 10,000/uL
o Undergoing invasive procedue 50,000/uL

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- Contains stable coagulation factors and plasma proteins (fibrinogen, antithrombin, albumin, proteins C and S)
- Indications
o Correction of coagulopathies, including the rapid reversal of warfarin
o Supplying deficient plasma proteins
o Treatment of thrombotic thrombocytopenic purpura

Fresh Frozen Plasma

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− Supplies fibrinogen, factor VIII, and von Willebrand factor (vWF)
− Each units contains 80 units Factor VIII
− Lesser volume than FFP

Cryoprecipitate

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− Contains Factor IX (hemophilia B)

Cryosupernate

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Adverse Reactions to Transfusion

♣ Immunologic
♣ Non-immunologic
♣ Infections

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prevention of blood loss

Hemostasis

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Stages of Hemostasis

1. Reflex Vasoconstriction
2. Primary Hemostasis
3. Secondary Hemostasis
4. Clot Retraction or Clot Dissolution

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♣ Results in immediate reduction in bleeding
♣ Mechanisms:
a. Local myogenic spasm– strongest contributor
b. Local autocoid factors from platelets and injured tissues e.g. Thromboxane A2, Endothelin (for ruptured blood vessel)
c. Nervous reflexes – from pain and other sensory impulses

Reflex Vasoconstriction

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♣ Formation of the primary thrombi or platelet plug
♣ Responsible for hemostasis of small vessels
♣ Involves platelets (key player), the blood vessel wall and von Willebrand factor (vWF)

Primary Hemostasis

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♣ Also called thrombocytes
♣ 1-4 μm, no nuclei and do not reproduce
♣ Originate from megakaryocytes
♣ Normal count: 150,000 to 450,000 per microliter
♣ Half-life: 8 to 12 days in the circulation
♣ Eventually cleared by macrophages in the blood and in the spleen

Platelet

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Stages in the Formation of the Platelet Plug

1. Platelet adhesion
2. Platelet activation
3. Platelet aggregation

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♣ Caused by low platelet count or abnormal platelet function
♣ Present as small hemorrhages in the skin and mucous membranes (small vessels)

Abnormality in Platelets

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♣ Initiates the coagulation cascade
♣ Can be explosive
♣ Limited by quantities of traumatized tissue, Factors X, VII and V
♣ Clotting can occur in 15 seconds

Extrinsic Pathway

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- Amplifies the cascade
- Slower, clotting in 1 to 6 minutes

Intrinsic Pathway

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In which part of the coagulation cascade does the extrinsic and intrinsic pathways converge?

Factor Xa-mediated generation of thrombin from prothrombin

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♣ Fibrin clot is invaded by fibroblasts which subsequently form connective tissue around the clot.
♣ Calcium from platelets stores also contribute to this
♣ As clot retracts, edges of the injured vessel are pulled together further reducing blood loss

Clot Retraction

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♣ Mediated by anticoagulant and thrombolytic mechanisms

Clot Dissolution

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What are other factors/molecules involved in the coagulation cascade?

Calcium, Vitamin K Anticoagulant Mechanisms

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involved in all steps in the cascade except the first 2 steps in the intrinsic pathway

Calcium

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required to produce prothrombin and other clotting factors in the liver

Vitamin K

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♣ Smooth endothelium
♣ Glycocalyx layer that repels platelets and clotting factors
♣ Thrombomodulin
- Secreted by the endothelium
- Binds thrombin thereby reducing free thrombin
- Activates Protein C which inactivates Factor V and VIII

Endothelium

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♣ 85 to 90% of the thrombin becomes adsorbed into the fibrin fibers
♣ Antithrombin III inactivates thrombin
♣ Heparin increases activity of antithrombin III hundredfold to thousandfold
Low concentrations in the body but is an extremely useful drug

Intravascular anticoagulants

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factor VIII deficiency

Hemophilia A

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factor IX deficiency

Hemophilia B

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is also known as immediate or anaphylactic hypersensitivity. The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 - 12 hours).

Type I hypersensitivity

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Immediate hypersensitivity is mediated by

IgE

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The primary cellular component in this hypersensitivity is the

Mast Cell or Basophil

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also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples.

Type II hypersensitivity

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Type II hypersensitivity is primarily mediated by antibodies of the

IgM or IgG classes and complement

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is also known as immune complex hypersensitivity. The reaction may be general or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.

Type III hypersensitivity

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They are mostly of the IgG class, although IgM may also be involved.

Type III hypersensitivity

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is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction (figure 5) which peaks 48 hours after the injection of antigen (PPD or old tuberculin).

Type IV hypersensitivity

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Blood loss anemia

Microcytic, hypochromic anemia

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Anemia where RBCs grow too large with odd shape

Megaloblastic Anemia

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Pathological condition caused by a genetic aberration in the hemocytoblastic cells that produce the red blood cells

Polycythemia Vera