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Hematology And Oncology > Physiology > Flashcards

Physiology Flashcards

1
Q

Universal donor of RBCs

Universal recipient of plasma

A

O

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2
Q

Hemophilia deficiency and type of inherited

A

Hemophilia A - 8 - XR
Hemophilia B - 9 - XR
Hemophilia C - 11 - AR

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3
Q

Coagulation steps that require calcium and phospholipids

A

Around activated 10

Around activated 7

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4
Q

Bradykinin function

A

Increases vasodilation, permeability and pain

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5
Q

Kinin cascade

A

HMWK to bradykinin via Kallikrein

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6
Q

XII to XIIa

A

Collagen, basement membrane, activated platelets, HMWK

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7
Q

Factor Xa inhibitors anticoagulants

A
  1. LMWH (greatest efficacy)
  2. Heparin
  3. Direct Xa inhibitors (apixaban, rivaroxaba)
  4. Fondaparinux
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8
Q

Thrombin inhibitors (anticoagulants)

A
  1. Heparin (greatest efficacy)
  2. LMWH (delteparin, enoxaparin)
  3. Direct thrombin inhibitors (argatroban, bivalirudin, dagigatran)
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9
Q

Universal recipient of RBCs

Universal donor of plasma

A

AB

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10
Q

Reduce vitamin K act as cofactor of

A

Precursor to mature 2, 7, 9, 10, C, S

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11
Q

vWF carries/protects

A

VIII

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12
Q

Pr C to activated Pr C

A

Thrombin- trombomodulin complex (endothelial cells)

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13
Q

Activated Pr C and Pr S cleaves and inactivates

A

Va and VIIIa

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14
Q

Antithrombin inhibits

A

Activated 2, 7, 9, 10, 11, 12

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15
Q

Heparin enhances the activity of

A

Antithrombin

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16
Q

Principles targets of antithrombin

A

Thrombin and factor Xa

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17
Q

Fibrinolyisis (by plasmin)

A
  1. Cleavage of fibrin mesh

2. Destruction of coagulation factora

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18
Q

Plasminogen to plasmin

A

tPA (used clinically as a thrombolytic)

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19
Q

Thrombolytics

A

tPA, alteplase, reteplase, streptokinase, tenecteplase

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20
Q

Inhibits plasmin formation

A

Aminocaproic acid

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21
Q

First response to endothelial damage

A

Transient vasoconstriction via neural stimulation reflex and endothelin (released from damaged cells)

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22
Q

Vwf are derived from

A
  1. Weibel-Palade bodies of endothelial cells

2. α-granules of platelets

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23
Q

Conformation changes after vwf binding in platelets via GpIb produce

A

Releasing of ADP , calcium, TXA2 (from platelet cycloxygenase)

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24
Q

ADP action on coagulation cascade

A
  • Platelets adherence to endothelium

- ADP binding receptor induce GpIIb/IIIa expression at platelet surface

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25
Pro-aggregation factors
1. TXA2 (released from platelets) 2. Decreased blood flow 3. Increased platelets aggregation
26
Anti-aggregation factors
1. PGI2 and NO (released by endothelial cells) 2. Increased blood flow 3. Decreased platelets aggregation
27
Bernand soulier disease
GpIb deficiency
28
ADP receptor inhibitors
1. Clopidogrel 2. Ticlopidine, 3. Prasurgel
29
Glanzman thrombasthenia
GpIIb/IIIa deficiency
30
GpIIb/IIIa inhibitors
Abciximab Eptifibatide Tirofiban
31
Ristocetin - mechanism of action
Activates vwf to bind GpIb
32
Bradykinin inhibitor
Ace
33
Factor 1
Fibrinogen
34
7 to 7a
Thromboplastin (tissue factor) | Ca2+
35
tPA inhibitor
Aminocaproic acid
36
Failure to platelets agglutination with ristocetin
Von willebrand disease | Bernarn soulier syndrome
37
Inside endothelial cells
``` Vwf and factor 8 Thromboplastin tPA PGI2 thrombomodulin (surface) ```
38
Rh hemolytic disease - mechanism
Rh- mothers exposed to fetal Rh+ blood (often during delivery) may make anti-D IgG --> in subsequent pregnancies, anti-D IgG (anti Rh) crosses placenta --> hemolytic disease of the newborn (erytrhoblastis fetalis) in the next Rh+ fetus
39
Hemolytic disease of newborn prevention
Administration of RhoCAM (anti-D Ig) during third semester and after pregnancy
40
Rh is AKA ...
D antigen
41
MC form of newborn hemolysis
ABO hemolytic disease of the newborn
42
ABO hemolytic disease of the newborn - usually occurs in / and mechanism
type 0 mother with a type A, B, or AB fetus | can occur in 1st pregnancy as maternal anti A and/or anti B IgG antibodies are formed early in life
43
ABO hemolytic disease of the newborn - future pregnancies
does not worsen
44
ABO hemolytic disease of the newborn - presentation
mild jundice in the neonate within 24h of birth
45
ABO hemolytic disease of the newborn - treatment
phototherapy or exchange transfusion
46
types of β-chain of hemoglobin
A: normal hemoglobyn β chain F: normal hemoglobin γ chain S: sickle cell hemoglobin β chain C: hemoglobin C β chain
47
On a gel of electrophoresis - hemoglobin migrates from ... to ...
negatively charged cathode --> positively charged anode
48
On a gel of electrophoresis - hemoglobins types according to migration (and why)
HbA migrates the farthest, followed by HbS, followed by HbC --> the missense mutationin HbS and HbC rplace glutamic acid (-) with valine (neutral) and lysine (+), respectively, impacting the net protein charge
49
hemoglobin - A, C, S, F - from anode to cathode
anode - A - F - S - C - cathode
50
beside its participation in kinin cascade, HMWK also
XII --> XIIa
51
coagulation intrinsic pathway - factors
12 --> 11 --> 9 (and then combined)
52
coagulation intrinsic pathway is AKA
contact
53
coagulation extrinsic pathway - factors
7 (and then combined)
54
coagulation extrinsic pathway is AKA
tissue factor pathway
55
combined pathway - factors
10 --> II (via 5) --> 1 + 13
56
X activation
- VIIa | - IXa + VIIIa
57
coagulation cascade - prothrombin is the factor ...
2
58
thrombin actions
- fibrinogen to fibrin monomers - XIII --> XIIIa - V --> Va - VIII --> VIIIa
59
coagulation cascade - combined pathway
X --> Xa Xa + Va --> prothrombin to thrombin thrombin --> fibrinogen to fibrin and XIII to XIIIa --> aggegation of fibrin + Ca2+ + XIIIa --> firin mesh stabilizes platelet plug
60
plasmin action
fibrin mesh --> fibrin degradation products
61
role of vitamin K in procoagulation
oxidized vit K --> reduced K (epoxide reductase) | --> act as a cofactor of γ-glutamyl trasnferase to 2, 7, 9, 10, C, S maturation
62
Warfarin inhibits
the enzyme vitamin K epoxide reductase
63
Neonates - procoagulation
lack enteric bacteria which produce vitamin K

Hematology And Oncology (21 decks)

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