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MM: Histology > Blood Detail > Flashcards

Blood Detail Flashcards

1
Q

Clotting factors are made where?

A

in the liver, except VIII (vascular endothelium)

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2
Q

intrinsic pathway

A

contact activation. blood contacts collagen. slower, forms larger clots

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3
Q

intrinsic pathway sequence

A

exposed collagen, XII, XI, IX, X

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4
Q

extrinsic pathway

A

tissue factor initiated. faster (15s), less thrombin, smaller clot

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5
Q

extrinsic pathway sequence

A

trauma, III, VII, X

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6
Q

exposed collagen–>

A

XII

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7
Q

XIIa–>

A

XI

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8
Q

XIa (or VII/TF)–>

A

IX/VIII/platelets

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9
Q

IX/VIII/platelets–>

A

V/X/platelets

X (prothrobin activator), V (from platelets)

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10
Q

damaged tissue–>

A

VII/TF

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11
Q

VII/TF–>

A

V/X/platelets (prothrombin activator)

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12
Q

V/X/platelets

A

FII (prothrombin)–> thrombin–>

FI (fibronogen) to fibrin

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13
Q

coagulation cascade is

A

secondary hemostatis

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14
Q

fibrin is

A

a woven rope of 3 chains (2 alpha, 2beta, 2 gamma) , acts as glue for platelets

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15
Q

fibrin ropes are crosslinked by

A

a transglutaminase, FXIIIa

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16
Q

Which CFs and anticoagulants depend on vitamin K?

A

FII, FVII, FIX, FX, Protein C and S

for binding Ca

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17
Q

Warfarin and Coumadin block

A

vitamin K, prevent clotting factors from attachment to platelets

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18
Q

Tenase complex

A

allows FX activation. IXa, VIIIa

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19
Q

IXa linked to

A

hemophilia B

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20
Q

VIIIa linked to

A

hemophilia A

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21
Q

circulating VII adheres to

A

non-endothelial cells that express Tissue Factor

which have become exposed to the blood due to damage. VII is then autoactivated

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22
Q

tertiary hemostatis: XII–>XIIa

A

cleaves kallirein, activating plasminogen to plasmin,

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23
Q

tertiary hemostatis: urokinase and tPA

A

also generate plasmin

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24
Q

plasmin

A

binds and deactivates V, VIII, fibrin to dissolve clots

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25
Q

detect clotting and clot reabsorption

A

fibrin degradation products (FDPs or d-dimers)

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26
Q

Protein C and S (with thrombomodulin)

A

inactivate FV and FVIII

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27
Q

platelets 150,000

A

normal

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28
Q

platelets 100,000

A

bleeding in surgery

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29
Q

platelets 20,000

A

bleeding in acute illness

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30
Q

platelets 10,000

A

spontaneous injury

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31
Q

WASp syndrome

A

X-linked disease (mainly males) thrombocytopenia, eczema, recurrent infections, and small-sized platelets

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32
Q

Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytopenia (XLT)

A

both caused by WASp mutation: thrombocytopenia and small platelets are the only consistent features of WAS and XLT

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33
Q

thrombocytopenia

A

relative decrease in platelets

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34
Q

GATA 1 and megakaryocytes

A

combines with RUNX1, drives gene expression. if defective, megakaryocytes do not mature

35
Q

Thrombopoetin

A

from liver, tells megakaryocytes to make platelets (via TPO receptor intereaction)

36
Q

congenital amegakaryocytic thrombocytopenia

A

defect in c-Mp1, Megakaryocyte’s Thrombopoetin receptor

37
Q

vWF A1 domain interacts where on platelet?

A

GpIba

38
Q

ADAMTS13

A

inhibits vWF clot size by cleaving at A2

39
Q

thrombotic thrombocytopenia purpura (TTP)

A

clots-low platelets-bleeing in skin. caused by ADAMTS13 mutations

40
Q

fibrin clots in TTP

A

shear RBCs into fragments called schistocytes

41
Q

platelet activation due to

A

Receptors for: TxA2, thrombin, ADP, and collagen integrin receptor

42
Q

TxA2 receptor

A

TxA2 receptor!

43
Q

PAR1

A

Thrombin receptor

44
Q

P2Y12

A

ADP receptor

45
Q

alpha2beta1, GPVI-FcR gamma

A

Collagen integrin recptor

46
Q

Aspirin

A

inhibits thromboxane sythesis.

limits platelet activation

47
Q

Plavix

A

irreversibly blocks P2Y12 receptor:

limits platelet activation

48
Q

P2Y12

A

ADP receptor on platelets, blocked by plavix (clopidogrel)

49
Q

Hermansky-Pudlak

A

platelets lack ADP granules. defective coat protein!

bleeding disorder, also comes with albinism

50
Q

alphaIIbB3

A

last step in activation. alphaIIbB3 integrin is activated, binds circulating fibrin/fibrinogen to stabilize clot.

51
Q

NO and prostaglandin PGI2

A

inhibit clotting.
bind plt., increase cAMP to decrease cytosolic Ca.
Generated by endothelium.

52
Q

In atherosclerosis, there is less

A

PGI2, thus more platelet activation

53
Q

LDL lipids activate

A

platelet thromboxane.

atherosclerosis is thrombogenic!

54
Q

platelet granules

A

serotonin, ADP, TxA2

55
Q

heme comes from

A

succinyl CoA. seven steps

56
Q

lead blocks

A

last step in heme formation

57
Q

RDS in heme formation

A

aminolevulinic acid step

58
Q

porphyria

A

heme abnormalities cause skin photosensitivity and psychiatric neural-visceral symptoms

59
Q

a2g2 or z2g2 or apha epsilon

A

embryonic hemoglobin

60
Q

ALPHA2GAMMA2, alpha2delta2

A

fetal hemoglobin

61
Q

ALPHA2BETA2, alpha2gamma2

A

adult hemoglobin

62
Q

thalassemia

A

defects in heme gene expression cause compensations that distort cell shape and half life of RBCs in circulation

63
Q

1 alpha mutation, aa/a-

A

asymptomatic

64
Q

2 alpha deletion aa/– or a-/a-

A

mild microcytic anemia

65
Q

microcytic anemia

A

characterized by small RBCs

66
Q

3 alpha deletion a-/–

A

anemia, hemolysis, jaundice. “hemoglobin H disease” beta tetramers precipitate and kill the cell

67
Q

4 alpha defects –/–

A

anemia, hydrops fetalis, death of fetus

68
Q

beta thal nomenclature

A

+ partial synthesis of beta chain

0 no synthesis of beta chain

69
Q

b/b0 or b/b+

A

asymptomatic

70
Q

b+/b0

A

intermediate thal trait

71
Q

b0/b0

A

severe thal

72
Q

thal traits

A

hypoxia, extramedullary hematopoesis, skull bone changes, iron overload. high output heart failure

73
Q

haptoglobin

A

captured heme released by lysed cells

74
Q

hemoglobinopathy

A

chains (not amounts) of hemoglobin defective

75
Q

SS disease

A

2 copies of beta6glu–>valine

76
Q

C disease

A

2 copies of beta6glu–>lysine

77
Q

SS and C disease results

A

polymerization of hemoglobin (exposed hydrophobic regions) short half-life, RBC destruction, bilirubin production causing gallstones, then anemia, hypoxia

78
Q

haptoglobin measure of

A

hemolysis

79
Q

blood maximum O2 load

A

20.4 ml/dl

80
Q

blood maximum O2 delivery

A

1020ml/min

81
Q

right shift on O2 curve

A

lower affinity, takes more O2 to saturate, thus more to deliver

82
Q

left shift on O2 curve

A

higher affinity, less delivery to tissue

83
Q

fetal hemoglobin has

A

higher affinity for O2 (duh, how else would it get O2)

leftward shift

84
Q

muscle O2 curve

A

even lefter than fetal!

MM: Histology (6 decks)

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