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Hemostasis Flashcards

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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

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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

Study These Flashcards
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

Study These Flashcards
A

Thrombocytopenia
Platelet dysfunction
von Willebrand disease

25
Causes of hemarthroses, hematuria, intramuscular/intracerebral/retroperitoneal hemorrhages
Severe hemophilia A/B Severe deficiencies of factors 7, 10, 13 Severe type 3 von Willebrand disease Afibrinogenemia
26
Causes of bleeding from stump of umbilical cord/habitual abortions
Afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, factor XIII deficiency
27
Petechiae
<3 mm non-blanching Often appear in clusters
28
purpura
3-10 mm | non-blanching
29
Ecchymosis
>1 cm bruise/contusion non-blanching
30
Hematoma
Localized collection of blood outside vessels, within tissue | raised swelling
31
Hemangioma
Abnormal buildup of blood vessels in the skin/interal organs
32
Senile purpura
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
Type I vWF disease
reduced vWF common m/c bleeding
34
Type 2 vWF disease
dysfunctional vWF protein uncommon m/c bleeding
35
type 3 vWF disease
no vWF and associated factor 8 deficiency rare severe m/c bleeding can see joint/muscle bleeding
36
Mild hemophilia
6-40% factor 8/9 bleeding only with trauma or surgery can present in adulthood
37
Moderate hemophilia
1-5% factor 8/9 bleeding usually with trauma or surgery can be spontaneous
38
Severe hemophilia
<1% factor 8/9 bleeding spontaneously or with minor trauma presents at a young age
39
vWF treatment
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
Hemophilia A tx
mild - desmopressin | recombinant factor 8
41
Platelet characteristics
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
Platelet contents
alpha granules: proteins associated with adhesions and clotting dense granules: calcium, ADP/ATP, serotonin no nucleus!
43
Normal platelet function
1) adhesion to vascular wall 2) secretion of granular contents 3) aggregation Procoagulant activity Vascular healing
44
Platelet adhesion
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
Platelet - secretion of granular contents
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
Platelet aggregation
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
Platelet procoagulant activity
Phospholipid required for 2 steps of clotting cascade Membranes of activated platelets provide phospholipid surface Bound fibrinogen helps localize clot
48
Qualitative platelet disorders
Congenital - platelet receptor deficiency, release/secretory defects, Granule content/storage pool disease Acquired - drugs, systemic conditions (renal failure, cardiopulmonary bypass), hematologic disease
49
PFA-100
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
Platelet disorders - reduced production
Congenital: rare Acquired: - nutritional - B12/folate - infiltrative - marrow failure - medication
51
Thrombocytopenia - sequestration
hypersplenism 1) congestive 2) reactive - infections, autoimmune hemolysis 3) infiltrative - benign (CT disease), malignant (hematologic)
52
Thrombotic thrombocytopenic purpura (TTP)
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
Classic pentad for TTP
``` Thrombocytopenia Microangiopathic hemolytic anemia Fever Neurologic symptoms and signs Renal impairment ``` Untreated - mortality 90%
54
TTP treatment
emergency! Plasma exchange Aspirin Corticosteroids for refractory disease/relapse Platelet transfusions are CONTRAINDICATED

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