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BMS200 > wk 11, lec 1 > Flashcards

wk 11, lec 1 Flashcards

1
Q

what is hemostasis

A

prevent blood loss in damage and also prevents excessive clot formation

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2
Q

3 things for hemostasis

A
  1. Vasospasm
  2. Platelet activation and formation of platelet plug
  3. Activate coagulation cascade and form fibrin
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3
Q

5 steps of clot formation

A
  1. Injury exposes collagen and thromboplastin
  2. Recruit platelets to site of injury to form temporary plug
  3. Platelets release 5-hydroxytryptamine (serotonin)  contraction and vasoconstriction
  4. Activate clotting cascade (because of collagen and thromboplastin)  activate thrombin which converts fibrinogen to fibrin monomers
  5. Fibrin monomers polymerize and cross link to form definitive clot
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4
Q

serotonin (5-hydroxytrypatamine) role in clot foramtion

A

contraction and vasoconstriction

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5
Q

what initiates coagulation and forms early fibrin plug vs what amplifies coagulation and forms more stable fibrin plug

i..e 1st activated and later activated

A
  • Extrinsic system: initiate coagulation and form early fibrin plug
    o Activated first
  • Intrinsic system: amplify coagulation and form more stable fibrin plug
    o Activated later
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6
Q

what are the 2 things the extrinsic system depends on

A

factor VIIa and TF (aka TPL and thromboplastin)

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7
Q

what do the intrinsic and extrinsic pathway lead to and via activation of what

A

final common pathway via activation of thrombin

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8
Q

how does thrombin get activated in final common pathway

A

o Factor Xa + factor Va + Ca2+

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9
Q

thrombin role in final common pathway

A

activate fibrin to stabilize clot

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10
Q

what are antithrombotic factors (ie.. inhibit platelet binding, secretion and aggregation)

A

Prostacyclin (PGI2), NO, ectoADPase/CD39

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11
Q

what are anticoagulant factors

A

Heparan proteoglycans, tissue-factor pathway inhibitor (TFPI), thrombomodulin

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12
Q

what is a firbonlytic enzyme

A

plasminogen activators

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13
Q

how does HSPG inhibit clotting

A
  • Heparan sulfate proteoglycan (HSPG) activates antithrombin (which inhibits IIa, IXa, Xa, XIa, XIIa)
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14
Q

what does thrombomodulin activate to inhibit clotting

A
  • Thrombomodulin activates protein C via thrombin (which inhibits Va, VIIIa)
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15
Q

where are platelet made

A
  • Made by megakaryocytes in bone marrow
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16
Q

what regulates platelets? what is this increased by

A

o Regulated by thrombopoietin
 Increased by IL-6 inflammation and low platelet #

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17
Q

structure of platelets

A
  • Anucleate cell fragments with mitochondria, cytoskeleton, secretory granules, receptors
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18
Q

where are platelets stored

A
  • 1/3 stored in spleen and released into circulation during hemorrhage
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19
Q

platelet lifespan

A

7-10 days

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20
Q

2 types of platelet granule

A

dense granules and alpha granule

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21
Q

what are platelet granules

A
  • Pre loaded vesicles or endosomes that are released when platelets are activated
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22
Q

what are in dense granules of platelets

A

o ADP (activate platelets), Ca2+ (co-factor to activate c.c), serotonin (vasoconstrict), polyphosphate (substrate to activate c.c)

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23
Q

what are the most abundant type of granules in platelets

A

alpha granules

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24
Q

what are in alpha granules

A

o Von Willebrand factors (vWF), factor V, fibrinogen, growth factors (FGF, VEGF, PDGF)
o Adhesive glycoproteins

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25
Q

what are the 3 platelet glycoproteins and what do they bind

A
  • GP Ib/IX- binds vWF
  • GP Ia/IIa- binds collagen under the endothelium
  • GPIIb/IIa –once activated; binds fibrinogen or vWF (stability of platelet plug)
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26
Q

platelet function when in healthy body

A

: endothelium secretes NO, prostacyclin, ADPase to prevent platelet activation
o Also hides collagen and vWF from circulating platelet GP receptors

27
Q

platelet function when endothelium injury

A

don’t secrete anti-platelet mediators and expose collagen and vWF

28
Q

steps in platelet function when injury

A
  1. Platelet release reaction (plateRR) is triggered: GP Ib/IX and Ia/IIa binds collagen and vWF  platelet adhesion to vessel wall
  2. PlateRR  release alpha and dense granules and activate GP IIb/IIa
  3. GP IIb/IIa binds fibrinogen  platelet aggregation
    - PlateRR leads to release of mediators for hemostasis
    o ADP (activates other platlets)
    o Serotonin and thromboxane (vasposasm)
    o Coagulation factors (increase fibrin production and aggregation)
    o Ca2+ and polyphosphate release (increase fibrin)
    - Platelets amplify coagulation via release of TF (tissue factor) vesicles and procoagulant microparticles
    - Platelets express P-selectin to increase leukocyte recruitment
    - Platelets have phospholipid surface and Ca2+ = needed for coagulation cascade
29
Q

what do platelets have on surface needed for coagulation cascade

A

phospholipid surface and ca2+

30
Q

what do platelets express to increase leukocyte recruitment

A

p selectin

31
Q

what do platelet amplify release of for coagulation cascade

A

of TF (tissue factor) vesicles and procoagulant microparticles

32
Q
  • GP Ib/IX- binds
A

vWF

33
Q
  • GP Ia/IIa- binds
A

collagen under the endothelium

34
Q
  • GPIIb/IIa –once activated; binds
A

fibrinogen or vWF (stability of platelet plug)

35
Q

PlateRR leads to release of what mediators

A

o ADP (activates other platelets)
o Serotonin and thromboxane (vasospasm)
o Coagulation factors (increase fibrin production and aggregation)
o Ca2+ and polyphosphate release (increase fibrin)

36
Q

extrinsic pathway

A
  • When injury; FVII is exposed to tissue factor (TF)  binds and forms FVIIa-TF complex
  • This activated FX  FXa
  • FXa activates prothrombin  thrombin  fibrinogen  fibrin
37
Q

intrinsic pathway

A
  • FXII comes in contact with negatively charged surface membrane (activated by platelets, collagen) and is activated into FXIIa (slowly)
    o complexed with heigh molecular weight kininogen (HMWK) -a protein expressed by activated platelets
  • FXIIa converts pre-kallikrein into kallikrein
    o positive feedback: kallikrein makes more FXIIa from factor XIIa (helps with slow process of above conversion)
  • HMWK-FXIIa complex activates FXI FXIa
  • FIxa complexes with FVIIIa to activate FC  FXa
    o Tenase= FIXa-FVIIIa-Ca2+ complex
  • FXa and FVa use Ca2+ to activate prothrombin  thrombin
38
Q

what is tense in intrinsic pathway

A

FIXa-FVIIIa-Ca2+ complex

39
Q

positive feedback loop of kallikrein in intrinsic pathway

A
  • FXIIa converts pre-kallikrein into kallikrein
    o positive feedback: kallikrein makes more FXIIa from factor XIIa (helps with slow process of above conversion)
40
Q

HMWK in what pathway

A

intrinsic path

41
Q

what do both the extrinsic and extrinsic pathway make for cross talk coagulation

A

FIXa

42
Q

what does thrombin activate in cross talk coagulation

A

o FV  FVa
o FVIII  FVIIIa
o FXI  FXIa
o Positive feedback on self and activate prothrombin
o XIII  XIIIa  cross link fibrin and stabilize clots

43
Q

how is FXII pro inflammatory (in intrinsic pathway)

A

o Activates kinin-kallikrein system  release bradykinin (vasodilate, increase, permeability, pain, muscle contraction)

o Cleave C3 and C5 (complement)

o Produce thrombin and fibrin split products (chemokine, COX, and platelet activating factor production = vasodilate, permeability, leukocyte emigration)

44
Q

how do platelet plugs recruit leukocytes

A

via p selection expression

45
Q

what does p selectin expression do in platelets

A

recruit leukocytes to:
o Modify PG synthesis
o More thrombin generation
o Optimal defense against microbes in blood

46
Q

3 things that decrease clot formation

A
  1. Downregulate platelet activation
    a. Via prostacyclin, NO, and ADPase –> inhibit PlateRR
  2. Downregulate coagulation cascade
  3. Fibrinolysis (destroy fibrin clots)
47
Q

3 things that will downrgulate platelet activation and inhibit PlateRR

A

prostacyclin, NO, and ADPase

48
Q

how to down regulate coagulation cascade (antithrombotic/ anticoagulation)

A
  1. antithrombin inhibits thrombin and some activated factors
  2. protein c (activated by thrombin)
  3. tissue factor pathway inhibitor (released via heparin)
49
Q

antithrombin does what to dowregualrate coagulation cascade

A
  • Antithrombin inhibits thrombin and activated factors IX, X, XI, XII
    o Heparin increases antithrombin activity
50
Q

protein c way to dowregualrate coagulation cascade

A
  • Protein C is activated by thrombin
    o Protein C + protein S = thrombomodulin  cleaves Va and VIIIa
51
Q

tissue factor pathway inhibitor can downregulate coagulation cascade by

A
  • Tissue factor pathway inhibitor is released in presence of heparin  inhibit activation of thrombin by TF and FVIIa
52
Q

in healthy tissue how does fibrinolytic system (dissolve fibrin clots)

A
  • Healthy endothelium: release tissue plasminogen activator (tPA), which activates plasminogen  plasmin
    o Plasmin degrades fibrin
    o Crosslinked fibrins produce D-dimers (fibrin degradation products) from fibrin proteolysis
53
Q

what degrades fibrin in healthy tissue

A

plain

54
Q

how to inhibit fibrinolysis

A

Plasminogen activator inhibtors (PAIs) block tPA activity
o Alpha-2 antiplasmin binds to plasmin

55
Q

labs for coagulation

A

-prothrombin time
-activated partial thromboplastin time
-thrombin time
-platelet count

56
Q

thrombin time lab tests for?

A

o Thrombin added- test for fibrinogen activity

57
Q

prothrombin time lab

what is added to blood sample

for what coagulation cascade

A

o International normalized ratio (INR)
o Time it takes to form clot via EXTRINSIC coagulation cascade
o Thromboplastin placed in blood sample and time to clot measured

58
Q

activated partial thromboplastin time lab

what is added to blood sample

for what coagulation cascade

A

o Time to clot via INTRINSIC cascade
o Phospholipids placed in blood sample and tome to clot measured

59
Q

which labs for intrinsic vs extrinsic cascade

A
  • Activated partial thromboplastin time (aPTT) = intrinsic
  • prothrombin time= extrinsic cascade
60
Q

which hemophilia is more common

A

hemophilia B

61
Q

hemophilia A vs hemophilia B which deficiency

A
  • Hemophilia A is FVII deficiency
  • Hemophilia B is FIX deficiency
62
Q

genes in hemophilia

A

x linked recessive

63
Q

presentation in hemophilias

A

defects in coagulation labs
o Severe spontaneous deep bleeds (i.e. into joints soft tissues and muscles)
o Hematuria

BMS200 (43 decks)

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