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Phisiology Hope > Hematology Physiology > Flashcards

Hematology Physiology Flashcards

1
Q

♣ 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

A

Blood Groups

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2
Q

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

A

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

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3
Q

Universal Donor

A

Blood Type O

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4
Q

Universal Recipient

A

Blood Type AB

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5
Q

♣ 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

A

Rh Blood Group

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6
Q

If you have the D antigen

A

Rh+

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7
Q

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

A

Rh-

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8
Q

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

A

Pretesting of Blood

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9
Q

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

A

Delayed hemolysis

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10
Q

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

A

Immediate hemolysis

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11
Q
  • Increases oxygen-carrying capacity and volume expansion

- Ideal for cases of acute hemorrhage of more than 25% of blood volume

A

Whole Blood

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12
Q
  • Increase oxygen-carrying capacity
  • Should only be given to those with anemia and symptoms
    o Dizziness
    o Increased heart rate
    o Difficulty of breathing
A

Packed Red Blood Cells

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13
Q
  • Reduces risk of mucosal bleeding
A

Platelet concentrates

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14
Q

Thresholds for transfusion of Platelet concentrates

A

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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15
Q
  • 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
A

Fresh Frozen Plasma

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16
Q

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

A

Cryoprecipitate

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17
Q

− Contains Factor IX (hemophilia B)

A

Cryosupernate

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18
Q

Adverse Reactions to Transfusion

A

♣ Immunologic
♣ Non-immunologic
♣ Infections

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19
Q

prevention of blood loss

A

Hemostasis

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20
Q

Stages of Hemostasis

A
  1. Reflex Vasoconstriction
  2. Primary Hemostasis
  3. Secondary Hemostasis
  4. Clot Retraction or Clot Dissolution
21
Q

♣ 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

A

Reflex Vasoconstriction

22
Q

♣ 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)

A

Primary Hemostasis

23
Q

♣ 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

A

Platelet

24
Q

Stages in the Formation of the Platelet Plug

A
  1. Platelet adhesion
  2. Platelet activation
  3. Platelet aggregation
25
Q

♣ Caused by low platelet count or abnormal platelet function

♣ Present as small hemorrhages in the skin and mucous membranes (small vessels)

A

Abnormality in Platelets

26
Q

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

A

Extrinsic Pathway

27
Q
  • Amplifies the cascade

- Slower, clotting in 1 to 6 minutes

A

Intrinsic Pathway

28
Q

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

A

Factor Xa-mediated generation of thrombin from prothrombin

29
Q

♣ 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

A

Clot Retraction

30
Q

♣ Mediated by anticoagulant and thrombolytic mechanisms

A

Clot Dissolution

31
Q

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

A

Calcium, Vitamin K Anticoagulant Mechanisms

32
Q

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

A

Calcium

33
Q

required to produce prothrombin and other clotting factors in the liver

A

Vitamin K

34
Q

♣ 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

A

Endothelium

35
Q

♣ 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

A

Intravascular anticoagulants

36
Q

factor VIII deficiency

A

Hemophilia A

37
Q

factor IX deficiency

A

Hemophilia B

38
Q

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).

A

Type I hypersensitivity

39
Q

Immediate hypersensitivity is mediated by

A

IgE

40
Q

The primary cellular component in this hypersensitivity is the

A

Mast Cell or Basophil

41
Q

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.

A

Type II hypersensitivity

42
Q

Type II hypersensitivity is primarily mediated by antibodies of the

A

IgM or IgG classes and complement

43
Q

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.

A

Type III hypersensitivity

44
Q

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

A

Type III hypersensitivity

45
Q

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).

A

Type IV hypersensitivity

46
Q

Blood loss anemia

A

Microcytic, hypochromic anemia

47
Q

Anemia where RBCs grow too large with odd shape

A

Megaloblastic Anemia

48
Q

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

A

Polycythemia Vera

Phisiology Hope (7 decks)

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