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Flashcards in Physiology Deck (63):
1

Universal donor of RBCs
Universal recipient of plasma

O

2

Hemophilia deficiency and type of inherited

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

3

Coagulation steps that require calcium and phospholipids

Around activated 10
Around activated 7

4

Bradykinin function

Increases vasodilation, permeability and pain

5

Kinin cascade

HMWK to bradykinin via Kallikrein

6

XII to XIIa

Collagen, basement membrane, activated platelets, HMWK

7

Factor Xa inhibitors anticoagulants

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

8

Thrombin inhibitors (anticoagulants)

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

9

Universal recipient of RBCs
Universal donor of plasma

AB

10

Reduce vitamin K act as cofactor of

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

11

vWF carries/protects

VIII

12

Pr C to activated Pr C

Thrombin- trombomodulin complex (endothelial cells)

13

Activated Pr C and Pr S cleaves and inactivates

Va and VIIIa

14

Antithrombin inhibits

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

15

Heparin enhances the activity of

Antithrombin

16

Principles targets of antithrombin

Thrombin and factor Xa

17

Fibrinolyisis (by plasmin)

1. Cleavage of fibrin mesh
2. Destruction of coagulation factora

18

Plasminogen to plasmin

tPA (used clinically as a thrombolytic)

19

Thrombolytics

tPA, alteplase, reteplase, streptokinase, tenecteplase

20

Inhibits plasmin formation

Aminocaproic acid

21

First response to endothelial damage

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

22

Vwf are derived from

1. Weibel-Palade bodies of endothelial cells
2. α-granules of platelets

23

Conformation changes after vwf binding in platelets via GpIb produce

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

24

ADP action on coagulation cascade

- Platelets adherence to endothelium
- ADP binding receptor induce GpIIb/IIIa expression at platelet surface

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