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HEMATOLOGY AND ONCOLOGY > HEMATOLOGY AND ONCOLOGY- Physiology > Flashcards

HEMATOLOGY AND ONCOLOGY- Physiology Flashcards

1
Q

What composes Blood group A?

A

A antigen on RBC surface and anti-B antibody in plasma

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2
Q

Which is the antigen of Blood group B?

A

B antigen on RBC surface

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3
Q

Whcih is the antibody of Blood group B?

A

anti A antibody in plasma

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4
Q

Which antigens do Blood group AB have on RBC surface?

A

A and B antigens on RBC surface

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5
Q

What kind of antibodies do AB blood group have?

A

No antibodies in plasma

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6
Q

“Universal recipient” of RBCs

A

AB blood groups

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7
Q

Which is the antibody of Blood group B?

A

anti A antibody in plasma

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8
Q

“Universal recipient” of RBCs

A

AB blood group

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9
Q

“Universal donor” of plasma

A

AB blood group

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10
Q

Which antigens does O blood group has?

A

Neither A nor B antigen on RBC surface

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11
Q

Which antibodies does O blood group has?

A

Both antibodies in plasma A and B

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12
Q

Which antibodies does O blood group has?

A

Both antibodies in plasma A and B

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13
Q

“Universal donor” of RBCs

A

O blood groups

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14
Q

“Universal recipient” of plasma

A

O blood groups

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15
Q

What can Incomplatible blood transfusions cause?

A

Immunologic response, hemolysis, renal failure, shock, and death

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16
Q

Do anti-A and anti-B antibodies-IgM cross the placenta?

A

No

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17
Q

Which antibodies are anti A and anti B antibodies?

A

IgM

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18
Q

Do anti-Rh- IgG cross the placenta?

A

Yes

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19
Q

Do anti-Rh- IgG cross the placenta?

A

Yes

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20
Q

Which antibodies does anti Rh has?

A

IgG

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21
Q

Where are Rh antigen?

A

On RBC surface

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22
Q

Where are Rh antigen?

A

On RBC surface

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23
Q

What happens in Rh disease?

A

Rh- mothers exposed to fetal Rh+ blood (often during delivery) may make anti-Rh IgG

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24
Q

What happens in subsequent pregnancies in Rh disease?

A

Anti-Rh IgG crosses the placenta, causing hemolytic disease (Erythroblastic fetalis) of the newborn in the next fetus that is Rh+

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25
Hemolytic disease of the newborn
Erythroblastic fetalis
26
Treatment for Rh disease
Rho (D) immune globulin for mother during every pregnancy to prevent initial sensitization of Rh- mother to Rh antigen
27
What happens in Hemophilia A?
Deficiency of factor VIII
28
What happens in Hemophilia B?
Deficiency of Factor IX
29
What activates bradykinin?
Kallikrein
30
What inactivates bradykinin
Angiotensin-converting enzyme (ACE)
31
What is the effect of epoxide reductase?
Acts in procoagulation | Converts Oxidized vitamin K → reduced vitamin K
32
What is the function of reduced vitamin K?
Acts as a cofactor in procoagulation
33
Vitamin K acts in the precursors of these coagulation factors
II, VII, IX, X, C, S
34
What does Warfarin inhibits?
The enzyme vitamin K epoxide reductase
35
What is the relationship of vitmain K and neonates?
Neonates lack enteric bacteria, which produces vitamin K
36
What happens in Vitmain K defiency?
↓ synthesis of factors II, VII, IX, X, protein C, protein S
37
Which coagulation factor is related to vWF?
vWF carries/ protects VIII
38
What activates Protein C?
Thrombin thrombomodulin complex
39
Where is Thrombin thrombomodulin complex produce?
In endothelial cells
40
What is the function of Protein S?
From activated protein C, cleaves and inactivates Va, VIIIa
41
What is the product of Plasminogen?
Plasmin
42
What activates Plasminogen?
Tissue plasminogen activator
43
What is the function of plasmin?
Fibrinolysis: 1. cleavage of fibrin mesh 2. destruction of coagulation factors
44
What is the function of Antithrombin?
Inhibits activated forms of factors II, VII, IX, X, XI, XII
45
Who enhances the activity of antithrombin?
Heparin
46
Principal targets of Antithrombin
Thrombin and Factor Xa
47
What do Factor V Leiden mutation leads to?
Produces a factor V resistant to inhibition by activated protein C
48
What is the function of Tissue plasminogen activator (tPA)?
Used clinically as a thrombolytic
49
Who manage primary hemostasis?
Platelet plug formation
50
Which is the process of platelet plug formation?
Injury → Adhesion → Activation → Aggreagation
51
Who mediates the injury phase of primary hemostasis?
vWF binds to exposed collagen upon endothelial damage
52
Who mediates the injury phase of primary hemostasis?
vWF binds to exposed collagen upon endothelial damage
53
Which is the first step of adhesion in primary hemostasis?
Platelets bind vWF via GpIb receptor at the site of injury only (specific)
54
In Adhesion phase of primary hemostasis, what happens next after platelets bind to vWF via GpIb receptor?
Platelets release ADP and Ca2+
55
What is the function of ADP and Ca2+ in Primary hemostasis?
Necessary for coagulation cascade
56
What is the function of ADP in primary hemostasis?
ADP helps platelets adhere to endothelium
57
What is the function of ADP in primary hemostasis?
ADP helps platelets adhere to endothelium
58
In primary activation what happens during activation phase?
ADP binding to receptor indices GpIIb/IIIA
59
What is the main event in Aggregation on primary hemostasis?
Fibrinogen binds GpIIb/IIIa receptors and links platelet
60
In primary hemostasis, who are pro-aggregation factors?
TXA2 ↓ Blood flow ↑ platelet aggregation
61
During primary aggregation, who are anti- aggregation factors?
PGI2 and NO ↑ blood flow ↓ platelet aggregation
62
Who release TXA2?
Platelets
63
During primary hemostasis, who release PGI2 and NO?
Endothelial cells
64
What is the final result of primary hemostasis?
Temporary plug stops bleeding
65
What is the final result of primary hemostasis?
Temporary plug stops bleeding
66
What is Thrombogenesis?
Formation of insoluble fibrin mesh
67
What is the main function of Aspirin?
Inhibits cyclooxygenase (TXA2 synthesis)
68
Inhibit ADP- induced expression of GpIIb/IIIa
Ticlopidine/ Clopidogrel
69
What is the effect of Ticlopidine/ Clopidogrel?
Inhibit ADP- induced expression of GpIIb/IIIa
70
What is the effect of Abciximab?
Inhibits GpIIb/IIIa directly
71
Inhibits GpIIb/IIIa directly
Abciximab
72
What is the effect of Ristocetin?
activates vWF to bind to GpIb
73
What other useful effect does Ristocetin has?
Useful for diagnosis: normal paltelet aggreagation response is not seen in von Willebrand disease
74
Irreversibly block ADP receptor
Clopidogrel and Ticlopidine
75
Deficiency of GpIb, who binds to vWF
Bernard Soulier syndrome
76
What is deficient in von Willebrand disease?
vWF
77
Precursor of TXA2
Arachidonic acid
78
Which factor promotes the conversion from arachidonic acid to TXA2?
COX
79
Deficiency of GpIIb/IIIa
Glanzmann thrombasthenia
80
What is erythrocyte sedminatation rate?
During acute phase reactants in plasma can cause RBC aggregation, thereby ↑ RBC sedimentation rate
81
Example of Acute phase reactatn
Fibrinogen
82
Who has higher density between plasma and RBC aggragates?
RBC aggregates
83
When is erythrocyte sedminatation rate increased?
Infections, autoimmune diseases (eg SLE, rheumathoid, rheumatoid arthritis, temporal arteritis), malignant neoplasms, GI disease (ulcerative colitis), pregnancy
84
When is erythrocyte sedminatation rate decreased?
Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia
85
When is erythrocyte sedminatation rate decreased?
Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia
86
When is erythrocyte sedminatation rate decreased?
Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

HEMATOLOGY AND ONCOLOGY (4 decks)

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