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MM: Histology > Blood Detail > Flashcards

Blood Detail Flashcards

(84 cards)

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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
detect clotting and clot reabsorption
fibrin degradation products (FDPs or d-dimers)
26
Protein C and S (with thrombomodulin)
inactivate FV and FVIII
27
platelets 150,000
normal
28
platelets 100,000
bleeding in surgery
29
platelets 20,000
bleeding in acute illness
30
platelets 10,000
spontaneous injury
31
WASp syndrome
X-linked disease (mainly males) thrombocytopenia, eczema, recurrent infections, and small-sized platelets
32
Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytopenia (XLT)
both caused by WASp mutation: thrombocytopenia and small platelets are the only consistent features of WAS and XLT
33
thrombocytopenia
relative decrease in platelets
34
GATA 1 and megakaryocytes
combines with RUNX1, drives gene expression. if defective, megakaryocytes do not mature
35
Thrombopoetin
from liver, tells megakaryocytes to make platelets (via TPO receptor intereaction)
36
congenital amegakaryocytic thrombocytopenia
defect in c-Mp1, Megakaryocyte's Thrombopoetin receptor
37
vWF A1 domain interacts where on platelet?
GpIba
38
ADAMTS13
inhibits vWF clot size by cleaving at A2
39
thrombotic thrombocytopenia purpura (TTP)
clots-low platelets-bleeing in skin. caused by ADAMTS13 mutations
40
fibrin clots in TTP
shear RBCs into fragments called schistocytes
41
platelet activation due to
Receptors for: TxA2, thrombin, ADP, and collagen integrin receptor
42
TxA2 receptor
TxA2 receptor!
43
PAR1
Thrombin receptor
44
P2Y12
ADP receptor
45
alpha2beta1, GPVI-FcR gamma
Collagen integrin recptor
46
Aspirin
inhibits thromboxane sythesis. | limits platelet activation
47
Plavix
irreversibly blocks P2Y12 receptor: | limits platelet activation
48
P2Y12
ADP receptor on platelets, blocked by plavix (clopidogrel)
49
Hermansky-Pudlak
platelets lack ADP granules. defective coat protein! | bleeding disorder, also comes with albinism
50
alphaIIbB3
last step in activation. alphaIIbB3 integrin is activated, binds circulating fibrin/fibrinogen to stabilize clot.
51
NO and prostaglandin PGI2
inhibit clotting. bind plt., increase cAMP to decrease cytosolic Ca. Generated by endothelium.
52
In atherosclerosis, there is less
PGI2, thus more platelet activation
53
LDL lipids activate
platelet thromboxane. | atherosclerosis is thrombogenic!
54
platelet granules
serotonin, ADP, TxA2
55
heme comes from
succinyl CoA. seven steps
56
lead blocks
last step in heme formation
57
RDS in heme formation
aminolevulinic acid step
58
porphyria
heme abnormalities cause skin photosensitivity and psychiatric neural-visceral symptoms
59
a2g2 or z2g2 or apha epsilon
embryonic hemoglobin
60
ALPHA2GAMMA2, alpha2delta2
fetal hemoglobin
61
ALPHA2BETA2, alpha2gamma2
adult hemoglobin
62
thalassemia
defects in heme gene expression cause compensations that distort cell shape and half life of RBCs in circulation
63
1 alpha mutation, aa/a-
asymptomatic
64
2 alpha deletion aa/-- or a-/a-
mild microcytic anemia
65
microcytic anemia
characterized by small RBCs
66
3 alpha deletion a-/--
anemia, hemolysis, jaundice. "hemoglobin H disease" beta tetramers precipitate and kill the cell
67
4 alpha defects --/--
anemia, hydrops fetalis, death of fetus
68
beta thal nomenclature
+ partial synthesis of beta chain | 0 no synthesis of beta chain
69
b/b0 or b/b+
asymptomatic
70
b+/b0
intermediate thal trait
71
b0/b0
severe thal
72
thal traits
hypoxia, extramedullary hematopoesis, skull bone changes, iron overload. high output heart failure
73
haptoglobin
captured heme released by lysed cells
74
hemoglobinopathy
chains (not amounts) of hemoglobin defective
75
SS disease
2 copies of beta6glu-->valine
76
C disease
2 copies of beta6glu-->lysine
77
SS and C disease results
polymerization of hemoglobin (exposed hydrophobic regions) short half-life, RBC destruction, bilirubin production causing gallstones, then anemia, hypoxia
78
haptoglobin measure of
hemolysis
79
blood maximum O2 load
20.4 ml/dl
80
blood maximum O2 delivery
1020ml/min
81
right shift on O2 curve
lower affinity, takes more O2 to saturate, thus more to deliver
82
left shift on O2 curve
higher affinity, less delivery to tissue
83
fetal hemoglobin has
higher affinity for O2 (duh, how else would it get O2) | leftward shift
84
muscle O2 curve
even lefter than fetal!

MM: Histology (6 decks)

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