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Emma Heme/Onc > Coagulation, Platelets, Bleeding Disorders, Thrombosis/Fibrinolysis > Flashcards

Coagulation, Platelets, Bleeding Disorders, Thrombosis/Fibrinolysis Flashcards

1
Q

vessel injury results

A 
vasoconstriction
exposure of subendothelium
-collagen/vWF
-recruitment of platelets
-primary platelet plug
TF:FVIIa
-thrombin gen
-form of fibrin clot
Fibrinolysis/wound healing
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2
Q

platelet adhesion

A

exposure of collagen which binds to vWF which binds GP1b on platelets

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3
Q

platelet aggregation

A

GP11b/IIIa
(fibrinogen receptor)

changes confirmation and enables binding

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4
Q

___ activates X and IX, which generates ___

A

TF:FVIIa activates X and IX, which generates THROMBIN

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5
Q

thrombin activates…

A

VIII
V
^ generate more thrombin

XIII
^crosslinks fibrin monomers

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6
Q

___ crosslinks fibrin monomers

A

XIII

a transglutaminase, activated by thrombin

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7
Q

vitamin K synthesizes…

A 
II
VII
IX
X
C/S
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8
Q

vitamin K sources

A

green leafy veggies

bacterial synthesis in gut

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9
Q

vitamin K is sctivated by ______ to its reduced form

A

vitamin K is sctivated by epoxide reductase to its reduced form

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10
Q

_____ is a cofactor for the γ-carboxylation of glutamic acid residues on various proteins required for blood clotting

A

vitamin K

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11
Q

____ inhibits vitamin K epoxide

A

WARFARIN inhibits vitamin K epoxide

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12
Q

____ –> plasminogen to plasmin –> fibrin to fibrin degradation products

A

tPa

released from endothelium

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13
Q

common path

A

fibrinogen, prothrombin (II), V, X

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14
Q

intrinsic path

A 
common path +
VIII
IX
XI
XII
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15
Q

extrinsic path

A

common path +

VII

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16
Q

lab test for intrinsic system

A

PTT

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17
Q

lab test for extrinsic system

A

PT

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18
Q

thrombin time

A

conversion of fibrinogen to fibrin clot

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19
Q

which two components of the coagulation cascade are not reflected in PT or PTT

A

vWF

XIII

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20
Q

platelets

origin

A

anucleate cells derived from megakaryotes in bone marrow

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21
Q

platelets

production regulation

A

GM-CSF, IL3, IL6, TPO

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22
Q

platelet circulation

A

circulating in INACTIVE state

7-10 d

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23
Q

alpha granules of platelets

A

fibrinogen
thrombospondin
vWF

V
PF4

beta thromboglobulin
platelet derived growth factor (PDGF)
P-selectin

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24
Q

platelet factor 4 (PF4)

A

heparin antagonist, promotes fibrin clot

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25
Q

P-selectin

A

adhesion of activated platelets to phagocytes

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26
Q

beta thromboglobulin

A

recruits fibroblasts

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27
Q

PDGF

A

recruits fibroblasts

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28
Q

dense granules of platelets

A

ADP
ATP
^platelet activation/recruitment

5HT
^vasoconstriction

Ca
^cofactor for clot

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29
Q

plasma membrane of platelets

A

GPIb
GPIa/IIa
GPIIb/IIIa

thrombin receptor
phospholipids

P-selectin
Fc receptor

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30
Q

vWF

A

binds to collagen in sub endothelium of damaged vessel wall

binds to GP1b on platelets

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31
Q

collagen in damaged vessel wall binds to platelet via

A

GPIa/IIa

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32
Q

platelet activating agents

A

EPI, ADP, collagen, thrombin

thromboxane A2, arachidonic acid

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33
Q

shape change of platelets

A

discoid to spherical w/ development of long pseudopods

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34
Q

tensase complex

A

IX, VIIIa, Xa

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35
Q

prothombinase complex

A

Xa, Va, II

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36
Q

PFA - 100

A

measures adhesion/aggregation

anti coagulated whole blood under high sheer rate passes thru aperture w/ 2 membranes coated in either collagen/EPI or collagen/ADP

closure time = time to clot form between 2 membranes

affected by thrombocytopenia/some anemia

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37
Q

bleeding time test

A

abnml in pt w/ mucocutaneous bleeding

vW disease, platelet disorders

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38
Q

Bernard Soulier disease

A

GP1b (vWF receptor)

  • abnml adhesion/agglutination
  • prolonged bleeding time
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39
Q

Glanzmann’s thrombasthenia

A

GPIIb/IIIa (fibrinogen receptor)

  • abnml aggregation and PFA-100
  • prolonged bleeding time
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40
Q

congenital thrombocytopathies

abnml platelet fxn

A

Bernard/soulier disease

Glanzmann’s thrombasthenia

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41
Q

acquired causes of thrombocytopathy

A

drugs (ASA, NSAIDs)
uremia
myeloproliferative disorders/myelodysplastic syndromes

42
Q

aspirin MOA includes (reversible or irreversible) COX inhibition

A

aspirin MOA includes IRREVERSIBLE COX inhibition

–> dec thromboxane –> dec aggregation

43
Q

NSAIDS MOA includes (reversible or irreversible) COX inhibition

A

NSAIDS MOA includes REVERSIBLE COX inhibition

–> dec thromboxane –> dec aggregation

44
Q

congenital thrombocytopenias

A 
May-Hegglin anomaly
Wiskott-Aldrich syndrome
Thrombocytopenia w/ absent radii (TAR)
Epstein's/Alport syndrome
Megakaryocytic hypOplasia/aplastic anemia
45
Q

May-Hegglin anomaly

A

AD, lg platelets, dole bodies in wbc

46
Q

Wiskott-Aldrich syndrome

A

XLR, eczema, immune dysfunction

47
Q

Thrombocytopenia w/ absent radii (TAR)

A

AR
abnml hand/wrist
cardiac lesions

48
Q

Epstein’s/Alport syndrome

A

AD, interstitial nephritis, deafness, lg platelets

49
Q

Megakaryocytic hypOplasia/aplastic anemia

A

stem cell disorder

may be acquired

50
Q

acquired causes of thrombocytopenia (dec production)

A

infiltrative process (malignancy)
viral (parvovirus, hepatitis)
drugs (chemo, alcohol, abs, anticonvulsants, antipsychotics)
Radiation

51
Q

acquired causes of thrombocytopenia (inc destruction)

A
  • heparin (HIT)
  • immune thrombocytopenia purport (ITP)
  • Thrombotic thrombocytopenia purpura (TTP)
  • Hemolytic Uremic Syndrome (HUS)
  • Disseminated intravascular coagulation (DIC)
  • Antiphospholipid antibody syndrome (APLA)
  • HELLP syndrome/pre-eclampsia
  • Hypersplenism
52
Q

immune thrombocytopenia purport (ITP)

A

AI disorder
Ab:Ag complex on surface of platelet targets it for removal of RES

comm cause: anti-GPIIB/IIIA Abs

ISOLATED platelet destruction

tx: immune modulation (steroids, IVIG, anti-D, Rituximab), TPO, splenectomy, adjunctive therapy for bleeding

53
Q

Thrombotic thrombocytopenia purpura (TTP)

A
  • adults
  • fever, thrombocytopenia, microangiopathic anemia, acute renal failure, neurologic dysfunction
  • dec activity of ADAMTS13 (vWF cleaving factor –> multimers of vWF build up –> platelet obstruction)
    -normal PT/PTT
    Tx: plasma exchange
54
Q

ISOLATED platelet destruction

A

immune thrombocytopenia purport (ITP)

55
Q

Hemolytic uremic syndrome (HUS)

A
  • children
  • diarrhea infection often E. coli strain
  • MAHA, thrombocytopenia, severe renal failure
  • normal PT/PTT
    Tx: supportive care (usu resolves on its own)
56
Q

Disseminated intravascular coagulation (DIC)

A
  • consumptive coagulopathy
  • thrombocytopenia, xs fibrinolysis, reduced coagulation fx –> hemorrhage, thrombosis, multiorgan failure
    causes: endotoxin, SEPSIS, tissue factor release, tissue injury, proteases, toxins, malignancy, obstetrical complications,
  • bleeding/thrombosis
  • prolonged PT/PTT, TT, dec fibrinogen, inc d-dimer
57
Q

___ is not measured by either PT or PTT, but it stabilizes _____, so could prolong PTT if low enough

A

vWF:Ag is not measured by either PT or PTT, but it stabilizes factor VIII, so could prolong PTT if low enough

58
Q

____ deficiency is a late step not involved in PT or PTT

A

FXIII deficiency

59
Q

inc PT, normal PTT

A

think VII

60
Q

PT is normal, PTTT is inc

A

think VIII, IX, X, XI, XII

61
Q

failure of mixing study to correct at 2 hrs implies..

A

pt has a circulating inhibitor protein

bc mixed pt plasma with pooled normal plasma containing normal coagulation fx

62
Q

thrombin time

A

measures conversion of fibrinogen to fibrin

prolonged: afibrinoginemia, dysfibrinoginemia, drugs (heparin)

63
Q

vWD

A
  • most comm congenital bleeding disorder
  • easy bruising, epistaxis, mucocutaneous bleeding, menorrhagia
  • usually AD, variable penetrance and expression
  • vWF normal range varies w/ blood type (lowest in O, highest in AB)
64
Q

blood type w/ lowest vWF

A

O

65
Q

blood type w/ highest vWF

A

AB

66
Q

vWF is stored in ____ (within endothelial cells)

A

Weibel-Palade bodies

67
Q

vWF is synthesized in

A

endothelial cells and megakaryocytes

68
Q

vWF is stored in ____ (within platelet alpha-granules)

A

megakaryocytes

69
Q

vWF is assembled and circulates as

A

multimers

lg multimers are most active in hemostasis in high shear vessels

70
Q

each monomer of vWF has binding sites for

A

VIII
GPIb
collagen
GPIIb/IIA

71
Q

2 functions of vWF

A
  1. mediates platelet-endothelium adhesion

2. stabilizes FVIII

72
Q

causes of acquired vWD

A

Abs (SLE, malignancy, myeloma, MGUS, infections, idiopathic)

hypOthyroidism (dec synthesis of vWF)

Cardiac (destruction of vWF (aortic stenosis, congenital heart disease, MV prolapse)

Drugs

73
Q

dx of vWD

A 
normal PT/PTT
(PTT possibly prolonged)
CBC/platelet/smear typically normal
PFA-100: abnml with EPI and ADP
VIII low if LOW vWF-Ag (range differs w/ blood type)
74
Q

vWD tx

A

DDAVP (desmopressin)
Factor VIII +vWF concentrates (human plasma)
Recombinant vW
Tx underlying condn if acquired

75
Q

adjunctive tx of vWF

A

antifibrinolytics
estrogens
AVOID NSAIDs/aspirin/herbal meds

76
Q

hemophilia A

A

XLR

  • carrier females can exhibit bleeding phenotype
  • VIII deficiency
  • inversions/deletions/point mut
77
Q

hemophilia B

A

“Christmas disease”
XLR
-carrier females can exhibit bleeding phenotype

78
Q

hemophilia clinical features

A

spontaneous hemarthoroses
IM bleeds
intracranial hemorrhage
mucocutaneous bleeds

sx occur within 1st yr of life

surgical bleeding and bleeding w/ trauma

target joints (sites of recurrent hemarthroses w/ hypertrophy of synovial sheath over time/painful arthritis)

79
Q

severe hemophilia fx levels

A

<1%

80
Q

very mild hemophilia fx levels

A

25-50%

81
Q

dx of hemophilia

A

PT - nml
PTT prolonged (VIII and FIX are intrinsic pathway)
mixing studies - nml at 0, 2 hr
factor assay to quantify factor levels

82
Q

Epsilon amino caproic acid (Amicar)

A

used for mucosal bleeding to inhibit plasminogen breakdown of the fibrin clot

83
Q

adjunctive therapy for hemophilia

A 
anti-fibrinolytics
epsilon amino caprice acid (amicar)
DDAVP
Protection, rest, ice, compression, elevation
pain cntrl (NOT NSAIDS)
Physical therapy
Ortho intervention
84
Q

DDAVP (desmopressin acetate)

A

releases FVIII and vWF from endothelial cells but only works if the patient makes enough factor VIII to be stored and released as in patients with MILD hemophilia A only.

does NOT work for FIX deficiency.

85
Q

complications of hemophilia

A
  • arthropathy
  • infection
  • inhibitors (polyclonal high affinity IgG Abs that neutralize infused FVIII –> bleeding continues. More common in severe hemophilia A)
86
Q

hemophilia pt w/ inhibitors

tx?

A

Bypass agents

  • recombinant VIIa
  • activated prothrombin complex concentrates

Suppression of inhibitors

  • immune tolerance induction: daily infusion of high dose factor
  • -> desensitization: induce tolerance of VIII or IX, stop prod of VIII or IX
  • effective in children but COSTLY
87
Q

hemophilia C

A

XI deficiency

  • Ashkenazi Jews
  • variable bleeding phenotype
  • bleeding after dental extraction
  • achieve hemostasis w/ prophylactic use of epsilon aminocaproic acid for mucosal bleeding
  • FFP or rFVIIa for bleeding
88
Q

acquired hemophilia

A

AutoAb to VIII
75% after 50 y/o

–Severe soft tissue bleeds 
–Less frequent hemarthroses
 –Spontaneous bleeding 
–Post-surgical bleeding
–Incidental finding of prolonged APTT
89
Q

tx of acquired hemophilia

A

tx underlying disease
immunosuppression
tx bleeding (DDAVP, VIII, rVIIa, FEIBA)

90
Q

FEIBA

A

prothrombin complex concentrate

91
Q

DIC testing

A

no one test, all are abnml

  • low platelets (often profound thrombocytopenia w/ bleeding)
  • prolonged PT and PTT
  • elevated D-dimer and fibrinopeptides
  • low fibrinogen
  • fragmented rbc (MAHA)
92
Q

DIC tx

A

tx bleeding (platelet transfusion, factor replacement (cryoprecipitate/FFP), heparin)

correct underlying disease

93
Q

liver disease –> bleeding

MOA?

A

Coagulopathy

  • hepatocyte dysfunc (dec V)
  • vitamin K deficiency
  • fibrinogen

Thrombocytopenia

  • hypersplenism
  • dec prod and abnml fxn

Failure to clear activated coagulation fx

  • DIC
  • elevated D-dimers
94
Q

hepatic cirrhosis is associated w/ ___ coagulopathy

A

SEVERE

  • deficiency of procoagulant proteins (prolonged PT/PTT)
  • deficiency of thrombopoietin (thrombocytopenia)
95
Q

Hemorrhagic disease of the newborn

A

vitamin K deficiency

  • gut relatively devoid of bacteria and hepatocytes are immature
  • vitamin K is given IM to all newborns to prevent bleeding in newborn period
96
Q

young woman w/ menorrhagia

FHx appears AD

A

vWF disease

97
Q

Virchow’s triad

A
  1. impaired blood flow
  2. circulating blood coagulation fx and inhibitors
  3. vascular damage
98
Q

mesenteric vein thrombosis

A

abd pain

99
Q

very ill pt w/ skin necrosis

A

DIC

100
Q

inherited thrombophilia causes

A

ATIII, protein C/S deficiency

APC, V Leiden, prothrombin mut

hyperhomocysteinemia

PAI-1 mut

elevated VIII, IX, XI, lipoproteins

101
Q

inherited thrombophilia

A

first thrombosis teen/early 20s
spontenous
high risk situations

Emma Heme/Onc (16 decks)

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