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2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Platelet plug formation

A

1) exposed collagen on subendothelial surface
2) GpIa/IIa and vWF binds, GpIbIX binds vWF
3) Platelet binds
4) Collagen activates PG synthesis within platelets –> TXA2 –> release of ADP, serotonin, fibrinogen, enzymes from intracellular granules
5) Released ADP and TXA2 causes platelet aggregation
6) GpIIbIIIa exposed, which binds fibrinogens, which binds other platelets

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2
Q

Fibrin clot formation (extrinsic)

A

1) vessel injury exposes TF - coagulation cascade
2) VIITF –> VIIa-TF
3) IX –> IXa and X –> Xa
4) Prothrombin –> thrombin (also catalyzed by Va)
5) Fibrinogen –> fibrin –> cross-linking

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3
Q

Intrinsic pathway

A

1) thrombin –> also VIII –> VIIIa
2) XI –> XIa
3) IX –> IXa
4) X –> Xa (also catalyzed by VIIIa)
etc

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4
Q

Clot termination

A

1) endothelial cells produce thrombomodulin, antithrombin, TFPI, tissue plasminogen activator 1, urokinase, plasminogen activator inhibitor, annexin 1
2) thrombomodulin binds thrombin, activates protein C and S, inactivates Va and VIIIa
3) Antithrombin inhibits factors VIIa, XIa, IXa, IIa (thrombin)
4) TFPI: inhibits protease, mainly VIIa/thrombin
5) plasminogen –> plasmin, cleaves fibrin clot

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5
Q

Immune thrombocytopenic purpura pathophys

A
  • increased platelet destruction due to abnormal IgG (commonly against GpIIbIIIa) - removed in RE system
  • idiopathic, may be seen with diseases like SLE
  • normal lifespan 7-10d, ITP few hours
  • insidious onset - petechial hemorrhage, easy bruising, menorrhagia
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6
Q

ITP Tx

A

Prednisolone
High dose IVIG for life-threatening hemorrhage
Immunosuppressive drugs
Rituximab
Splenectomy (if refractory disease)
Platelet transfusion (only lasts few h - ineffective)

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7
Q

Secondary thrombocytopenia pathophys

A 
Increased platelet destruction
HIV infection
H. pylori
CLL, Hodgkin's lymphoma
AIHA
SLE
Drug-induced
post-transfusion
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8
Q

Aspirin-induced thrombocytopenia pathophys

A

Inhibition of COX1 and 2 –> reduced TXA2 synthesis

consequent impairment of platelet aggregation

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9
Q

von Willebrand disease pathophys

A

Most often autosominal dominant with variable penetrance
Normally produced in megakaryocytes and endothelial cells
Roles:
- promotes platelet adhesion to subendothelium at high shear rates
- carrier for VIII

Typically see mucocutaneous bleeding
Rarely see hemarthrosis/muscle hematoma

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10
Q

Hemophilia A pathophys

A

VIII deficiency

synthesized in liver/endothelium

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11
Q

Tx hemophilia A

A

factor VIII replacement

DD-arginine vasopressin with fluid restriction

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12
Q

Hemophilia B

A

Factor IX deficiency
vitamin K dependent

Tx: recombinant IX replacement

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13
Q

Vitamin K deficiency pathophys

A

Fat-soluble vitamin
Obtained from green vegetables & gut bacteria
Inadequate diet/malabsorption/inhibition by drugs (warfarin)
Role in gamma-carboxylation of glutamic acid in coagulation factors (allows factors to bind Ca and attach to platelet PL)

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14
Q

Liver disease hemostatic disease pathphys

A

Vitamin K-dependent factor deficiency (II, VII, IX, X, protein C)
factor V, fibrinogen deficiency (severe)
thrombocytopenia from hypersplenism/ immune complex-mediated platelet destruction
Dysfibrinogemia

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15
Q

DIC (disseminated intravascular coagulation) pathophys

A

Widespread intravascular deposition of fibrin with consumption of coagulation factors and platelets
Consequence of abnormal release of procoagulants, endothelial damage, or platelet aggregation due to:
- infection
- malignancy
- hypersensitivity
- widespread tissue damage (surgery, trauma, burn)
Overwhelm normal removal
Excessive fibrin monomer formation - binds fibrinogen, leading to coagulation defect
Intense fibrinolysis by thrombin –> coagulation defect

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16
Q

Heparin use thrombocytopenia pathophys

A

HIT
PF4 in alpha granules secreted upon platelet activation –> binds heparin –> complex is immunogenic
IgG-heparin-FP4 binds platelet surfaces, causes platelet activation, degranulation and platelet aggregation
1-5% patients
4-14 days after initiation of therapy

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17
Q

Lupus anticoagulant pathophys

A

Antiphospholipid Ab associated with venous/arterial thromboses
Activates and stimultaes coagulation cascade
- pathologic thromboses of arteries and veins
- possible placental infarct and pregnancy loss
Associated with antiphospholipid antibody syndrome

Anticoagulant IN VITRO
Procoagulant IN VIVO

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18
Q

Primary hemostasis PE

A

Mucocutaneous bleeding

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19
Q

Secondary hemostasis PE

A

Deep tissue bleeding

Hemarthrosis, muscle hematoma

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20
Q

Elevated PTT

A

Problem in the intrinsic pathway

  • Factor 8, 9, 11, 12, vWF deficiency
  • 12 does not cause bleeding
  • 11 rare
  • 8/9 X-linked
  • 8 carried by vWF so would be low in 8 def/VWD

Coagulation factor inhibitor - lupus anticoagulant, heparin, acquired factor 8 inhibitor

Followup with mixing study (50:50)

  • if corrected: factor def
  • if remains elevated: inhibitor present
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21
Q

Elevated PT

A

problem in extrinsic pathway

factor 7 deficiency

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22
Q

Elevated PTT and PT

A 
Problem in the common pathway/ fibrinogen
Common: 1, 2, 5, 10
Multiple factors: 12, 11, 9, 8, 7
- hemophilia A (8), B (9) 
- vitamin K: 2,7, 9, 10
- liver disease (TT not prolonged)
- DIC

give vit K to differentiate between liver disease & vitamin K

23
Q

Key questions for hematologic problem

A 
Bleeding site
Age of onset
Consistency of bleeding problem
Spontaneous or provoked by trauma
Previous medical procedures/transfusions
Severity
24
Q

Cause of mucocutaneous bleeding

A

Thrombocytopenia
Platelet dysfunction
von Willebrand disease

25
Q

Causes of hemarthroses, hematuria, intramuscular/intracerebral/retroperitoneal hemorrhages

A

Severe hemophilia A/B
Severe deficiencies of factors 7, 10, 13
Severe type 3 von Willebrand disease
Afibrinogenemia

26
Q

Causes of bleeding from stump of umbilical cord/habitual abortions

A

Afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, factor XIII deficiency

27
Q

Petechiae

A

<3 mm
non-blanching
Often appear in clusters

28
Q

purpura

A

3-10 mm

non-blanching

29
Q

Ecchymosis

A

> 1 cm
bruise/contusion
non-blanching

30
Q

Hematoma

A

Localized collection of blood outside vessels, within tissue

raised swelling

31
Q

Hemangioma

A

Abnormal buildup of blood vessels in the skin/interal organs

32
Q

Senile purpura

A

extremely common in old age
age-dependent deterioration of the vascular supporting structure
bruising on the dorsum of the hands and forearms
serious bleeding does not occur

33
Q

Type I vWF disease

A

reduced vWF
common
m/c bleeding

34
Q

Type 2 vWF disease

A

dysfunctional vWF protein
uncommon
m/c bleeding

35
Q

type 3 vWF disease

A

no vWF and associated factor 8 deficiency
rare
severe m/c bleeding
can see joint/muscle bleeding

36
Q

Mild hemophilia

A

6-40% factor 8/9
bleeding only with trauma or surgery
can present in adulthood

37
Q

Moderate hemophilia

A

1-5% factor 8/9
bleeding usually with trauma or surgery
can be spontaneous

38
Q

Severe hemophilia

A

<1% factor 8/9
bleeding spontaneously or with minor trauma
presents at a young age

39
Q

vWF treatment

A

1) Desmopressin - release endogeneous stores (WPB)
- usually 3-5x rise in vWF and factor 8 in type 1, but not in types 2 and 3
2) exogenous vWF - donor plasma, usually for types 2/3, also give factor 8

40
Q

Hemophilia A tx

A

mild - desmopressin

recombinant factor 8

41
Q

Platelet characteristics

A

New platelets are larger
Up to 1/3 are sequestered in the spleen - 90% if splenomegaly
Normal life span 7-10 d
Removal: 50% by the spleen, 33% by the liver, 17% by bone marrow/lymph node/other tissues

42
Q

Platelet contents

A

alpha granules: proteins associated with adhesions and clotting
dense granules: calcium, ADP/ATP, serotonin
no nucleus!

43
Q

Normal platelet function

A

1) adhesion to vascular wall
2) secretion of granular contents
3) aggregation

Procoagulant activity
Vascular healing

44
Q

Platelet adhesion

A

1) GpIaIIa engages exposed collagen in subendothelium
2) subendothelial microfibrils bind vWF, which binds platelet GpIbIX
3) platelets become more spherical, extrude pseudopods, form a monolayer

45
Q

Platelet - secretion of granular contents

A

1) collagen exposure activates TXA2 synthesis
2) activation of phospholipase C –> increased calcium concentrations within platelet –> granules released
3) releases ADP, serotonin, fibrinogen, enzymes
4) triggers further conformational change and activation

46
Q

Platelet aggregation

A

1) GpIbIX binding –> activation of GIIbIIIa, exposing binding sites for fibrinogen
2) fibrinogen binds platelets to one another
3) ADP and TXA2 (also a potent vasoconstrictor) recruit other platelets

47
Q

Platelet procoagulant activity

A

Phospholipid required for 2 steps of clotting cascade
Membranes of activated platelets provide phospholipid surface
Bound fibrinogen helps localize clot

48
Q

Qualitative platelet disorders

A

Congenital - platelet receptor deficiency, release/secretory defects, Granule content/storage pool disease

Acquired - drugs, systemic conditions (renal failure, cardiopulmonary bypass), hematologic disease

49
Q

PFA-100

A

Platelets - add agonist –> measure light transmission
If platelets aggregate and sink to the bottom, 100% light transmission at the top

will be abnormal in someone taking ASA/NSAIDs, vWF disease, congenital platelet function defects

50
Q

Platelet disorders - reduced production

A

Congenital: rare

Acquired:

  • nutritional - B12/folate
  • infiltrative
  • marrow failure
  • medication
51
Q

Thrombocytopenia - sequestration

A

hypersplenism

1) congestive
2) reactive - infections, autoimmune hemolysis
3) infiltrative - benign (CT disease), malignant (hematologic)

52
Q

Thrombotic thrombocytopenic purpura (TTP)

A

Thrombotic microangiopathies
Microvascular occlusive disorders
Triggered by: HUS, congenital/autoantibody causes of ADAMTS13 deficiency (familial TTP)
Normally ADAMTS13 cleaves large vWF; uncleaved –> attracts platelets

53
Q

Classic pentad for TTP

A 
Thrombocytopenia
Microangiopathic hemolytic anemia
Fever
Neurologic symptoms and signs
Renal impairment

Untreated - mortality 90%

54
Q

TTP treatment

A

emergency!
Plasma exchange
Aspirin
Corticosteroids for refractory disease/relapse
Platelet transfusions are CONTRAINDICATED

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