Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematology And Oncology > Physiology > Flashcards

Physiology Flashcards

1
Q

Universal donor of RBCs

Universal recipient of plasma

A

O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hemophilia deficiency and type of inherited

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Coagulation steps that require calcium and phospholipids

A

Around activated 10

Around activated 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bradykinin function

A

Increases vasodilation, permeability and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Kinin cascade

A

HMWK to bradykinin via Kallikrein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

XII to XIIa

A

Collagen, basement membrane, activated platelets, HMWK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Factor Xa inhibitors anticoagulants

A
  1. LMWH (greatest efficacy)
  2. Heparin
  3. Direct Xa inhibitors (apixaban, rivaroxaba)
  4. Fondaparinux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Thrombin inhibitors (anticoagulants)

A
  1. Heparin (greatest efficacy)
  2. LMWH (delteparin, enoxaparin)
  3. Direct thrombin inhibitors (argatroban, bivalirudin, dagigatran)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Universal recipient of RBCs

Universal donor of plasma

A

AB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Reduce vitamin K act as cofactor of

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vWF carries/protects

A

VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pr C to activated Pr C

A

Thrombin- trombomodulin complex (endothelial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Activated Pr C and Pr S cleaves and inactivates

A

Va and VIIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antithrombin inhibits

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Heparin enhances the activity of

A

Antithrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Principles targets of antithrombin

A

Thrombin and factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fibrinolyisis (by plasmin)

A
  1. Cleavage of fibrin mesh

2. Destruction of coagulation factora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Plasminogen to plasmin

A

tPA (used clinically as a thrombolytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Thrombolytics

A

tPA, alteplase, reteplase, streptokinase, tenecteplase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Inhibits plasmin formation

A

Aminocaproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

First response to endothelial damage

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vwf are derived from

A
  1. Weibel-Palade bodies of endothelial cells

2. α-granules of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Conformation changes after vwf binding in platelets via GpIb produce

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ADP action on coagulation cascade

A
  • Platelets adherence to endothelium

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pro-aggregation factors

A
  1. TXA2 (released from platelets)
  2. Decreased blood flow
  3. Increased platelets aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Anti-aggregation factors

A
  1. PGI2 and NO (released by endothelial cells)
  2. Increased blood flow
  3. Decreased platelets aggregation
27
Q

Bernand soulier disease

A

GpIb deficiency

28
Q

ADP receptor inhibitors

A
  1. Clopidogrel
  2. Ticlopidine,
  3. Prasurgel
29
Q

Glanzman thrombasthenia

A

GpIIb/IIIa deficiency

30
Q

GpIIb/IIIa inhibitors

A

Abciximab
Eptifibatide
Tirofiban

31
Q

Ristocetin - mechanism of action

A

Activates vwf to bind GpIb

32
Q

Bradykinin inhibitor

A

Ace

33
Q

Factor 1

A

Fibrinogen

34
Q

7 to 7a

A

Thromboplastin (tissue factor)

Ca2+

35
Q

tPA inhibitor

A

Aminocaproic acid

36
Q

Failure to platelets agglutination with ristocetin

A

Von willebrand disease

Bernarn soulier syndrome

37
Q

Inside endothelial cells

A 
Vwf and factor 8 
Thromboplastin 
tPA
PGI2
thrombomodulin (surface)
38
Q

Rh hemolytic disease - mechanism

A

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
Q

Hemolytic disease of newborn prevention

A

Administration of RhoCAM (anti-D Ig) during third semester and after pregnancy

40
Q

Rh is AKA …

A

D antigen

41
Q

MC form of newborn hemolysis

A

ABO hemolytic disease of the newborn

42
Q

ABO hemolytic disease of the newborn - usually occurs in / and mechanism

A

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
Q

ABO hemolytic disease of the newborn - future pregnancies

A

does not worsen

44
Q

ABO hemolytic disease of the newborn - presentation

A

mild jundice in the neonate within 24h of birth

45
Q

ABO hemolytic disease of the newborn - treatment

A

phototherapy or exchange transfusion

46
Q

types of β-chain of hemoglobin

A

A: normal hemoglobyn β chain
F: normal hemoglobin γ chain
S: sickle cell hemoglobin β chain
C: hemoglobin C β chain

47
Q

On a gel of electrophoresis - hemoglobin migrates from … to …

A

negatively charged cathode –> positively charged anode

48
Q

On a gel of electrophoresis - hemoglobins types according to migration (and why)

A

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
Q

hemoglobin - A, C, S, F - from anode to cathode

A

anode - A - F - S - C - cathode

50
Q

beside its participation in kinin cascade, HMWK also

A

XII –> XIIa

51
Q

coagulation intrinsic pathway - factors

A

12 –> 11 –> 9 (and then combined)

52
Q

coagulation intrinsic pathway is AKA

A

contact

53
Q

coagulation extrinsic pathway - factors

A

7 (and then combined)

54
Q

coagulation extrinsic pathway is AKA

A

tissue factor pathway

55
Q

combined pathway - factors

A

10 –> II (via 5) –> 1 + 13

56
Q

X activation

A
  • VIIa

- IXa + VIIIa

57
Q

coagulation cascade - prothrombin is the factor …

A

2

58
Q

thrombin actions

A
  • fibrinogen to fibrin monomers
  • XIII –> XIIIa
  • V –> Va
  • VIII –> VIIIa
59
Q

coagulation cascade - combined pathway

A

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
Q

plasmin action

A

fibrin mesh –> fibrin degradation products

61
Q

role of vitamin K in procoagulation

A

oxidized vit K –> reduced K (epoxide reductase)

–> act as a cofactor of γ-glutamyl trasnferase to 2, 7, 9, 10, C, S maturation

62
Q

Warfarin inhibits

A

the enzyme vitamin K epoxide reductase

63
Q

Neonates - procoagulation

A

lack enteric bacteria which produce vitamin K

Hematology And Oncology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions