adiuvante Dei gratia doctorum factionis 2014-2015

HEMATOLOGY: COAGULATION DRA SAMSON-CRUZ

DISORDERS

SECONDARY HEMOSTASIS plasmin. Any free plasmin is complexed with α2 plasmin

inhibitor (α2PI). Fibrin is degraded to low-molecular-weight
fragments, fibrin degradation products (FDPs).

 Plasmin can also degrade fibrinogen

 Localized reaction:
 tPA and some uPA activate plasminogen
more effectively when it is adsorbed to fibrin
clots
 Plasmin that enters the circulation is rapidly
bound and neutralized by the alpha 2
plasmin inhibitor
 EC release plasminogen activator inhibitor 1
Figure 1. Steps in secondary hemostasis (this part was not which blocks the action of tPA
discussed by doc)
INHIBITORS
FIBRINOLYTIC SYSTEM Antithrombin
 begin immediately after the formation of definitive  forms complexes with all serine protease coagulation
hemostatic plug factors except factor VII
 3 potential activators  rates of complex formation are accelerated by
 Hageman factor fragments heparin and heparin-like molecules on the surface of
 uPA the endothelial cells
 tPA  Heparin's ability to accelerate antithrombin activity is
the basis for its anticoagulant action
Protein C
 converted to an active protease by thrombin after it is
bound to an endothelial cell protein called
thrombomodulin
 apC then inactivates plasma cofactors V and VIII,
which slows down two critical coagulation reactions
 stimulate the release of tPA from endothelial cells
Protein S
 enhance the inhibitory function of protein C

FIBRINOLYTIC SYSTEM

Figure 3. The contribution of the tissue factor–VIIa complex

Figure 2. A schematic diagram of the fibrinolytic pathway. (TF-VIIa) and tissue factor pathway inhibitor (TFPI) to
Tissue plasminogen activator (tPA) is released from endothelial coagulation. Initial activation of factor IX by TF-VIIa
cells, enters the fibrin clot, and activates plasminogen to compensates for deficiencies in the early factors, e.g., factors
XII and XI. The subsequent inhibition of TF-VIIa by TFPI makes

 ISTEPANIA
sustained activation of factor X by IXa and VIIIa critical for cartilage and lead to chronic joint deformity and limited
normal hemostasis. PL, phospholipid. mobility

BLOOD CLOT
RED THROMBI
 veins
 rich in fibrin and trapped red cells and contain
relatively few platelets
 can break off and embolize to pulmonary circulation
WHITE THROMBI
 arteries
 predominantly composed of platelets and have little
fibrin
 may readily dislodged from arterial wall and embolize  Intramuscular bleeding in haemophilia A
to distant sites causing permanent or temporary  Subcutaneous and deep intramuscular bleeding into
ischemia the buttock in haemophilia A
 common cause of embolism in the cerebral and
retinal circulation
hemostatic plugs
 physiologic response to injury
 very similar to pathologic thrombi
thrombosis
 coagulation occurring in the wrong place or at the
wrong time

HEMOPHILIAS
CLINICAL EVALUATION
HISTORY
 hemostatic disorder or by a local anatomic defect
 following common hemostatic stresses
 family history of bleeding
 bleeding occurs hours or days after injury and is
unaffected by local therapy
 occurs in deep subcutaneous tissues, muscles, joints,  Haemarthrosis in haemophilia A
or body cavities  Haemorrhage of one knee joint (haemarthrosis) in
 hemophilias are inherited forms that are deficient in haemophilia A.
factor 8 and 9
 sex linked abnormality in X chromosome
 dec factor 8 and 9 -> bleeding tendencies
 hemophilia A depends on factor VIII levels
 if severe hemophilia is seen in childhood, patient
manifests hematomas and abnormal bleeding
tendencies
MANIFESTATIONS
 Bleeding into body cavities, the retroperitoneum, or
 Haemarthroses in haemophilia A
joints
 Small bruises and bilateral haemorrhage into the knee
 Repeated joint bleeding
joints (haemarthroses) in haemophilia A
 Joint deformities
 necrosis of tissues or nerve compression
 In patients who presents manifestations require
family history and then request for CBC, platlet,PT,
Retroperitoneal hematomas can cause femoral nerve
PTT and BT
compression, and large collections of poorly coagulated blood
 Usually hemophilias have elongated PTT
in soft tissues occasionally mimic malignant growths — the
 Once seen, request for specific factor assay
pseudotumor syndrome
to know whether it is factor 8 or 9 because
they have the same clinical manifestation
Repeated joint bleeding may cause synovial thickening, chronic
inflammation, and fluid collections and may erode articular
  Treatment failure happens if inhibitors are formed,  congestive heart failure
meaning antibodies are formed, thus patient thus not  Malignancy
respond to treatment   Immobility
 inherited coagulation abnormalities induce a
COAGULATION FACTORS LOOKED FOR EACH TEST hypercoagulable or prethrombotic state and
predispose patients to thrombosis
 affect young people
 cause recurrent episodes of
thromboembolism
 may involve multiple members of a single
family

HEMOPHILIA A/FACTOR VIII DEFICIENCY

PATHOGENESIS
 factor VIII coagulant protein
 large (265-kDa), single-chain protein
SCREENING TEST FOR FACTOR VIII  regulates the activation of factor X by
UREA CLOT LYSIS TEST proteases generated in the intrinsic
coagulation pathway
 fibrin that has not been cross-linked will dissolve in  synthesized in liver and circulates complexed
urea, whreas fibrin that has been cross-linked by the to the vWF protein
action of factor XIII will not  present in low conc (10 ug/L) and is
 small amount of plasma that has been clotted is susceptible to proteolysis
placed in a solution of urea, identical clot is placed in  gene for factor VIII is on the X chromosome
saline as a control; both incubated overnight and  1 in 10,000 males is born with deficiency or
compared. Dissolution of clot in urea soln confirms dysfunction of the factor VIII molecule
factor XIII deficiency
MIXING TEST CLINICAL MANIFESTATIONS
 performed if screening test is prolonged  bleeding into soft tissues, muscles, and weight-
 mixing equal amounts of patients plasma and a bearing joints
known normal plasma and determining if normal  clinical severity and plasma AHF level
plasma corrects the defect  severe disease
 with correction factor deficiency o <1% factor VIII activity
 w/o correction ab to coagulation factor o bleed frequently even without
discernible trauma
DISORDERS OF COAGULATION AND THROMBOSIS  moderate disease
Congenital plasma coagulation defects o 1 to 5% factor VIII activity
 defects in single coagulation proteins o less frequent bleeding episodes
 may have severe bleeding and chronic disability and  mild disease
require specialized medical therapy o >5% factor VIII activity
 prolong either PT PTT o infrequent bleeding that is usually
 quantitative assays of specific coagulation proteins secondary to trauma
 interval range 50 to 150%  ~25% discovered when they bleed after major trauma
 minimal level of most individual factors needed for or surgery
adequate hemostasis is 25%  majority of patients have factor VIII levels <5%
Acquired coagulation disorders  Hemophilic bleeding
 more complex  occurs hours or days after injury
 arising from deficiencies of multiple coagulation  can involve any organ
proteins
 if untreated, may continue for days or weeks
 affecting both primary and secondary hemostasis
 compartment syndromes, pseudophlebitis
 most common acquired hemorrhagic disorders are
 pseudotumor syndrome
(1) disseminated intravascular coagulation (DIC)
 extensive cephalhematoma or profuse bleeding at
(2) the hemorrhagic diathesis of liver disease
circumcision
(3) vit K def and complications of anticoagulant tx
 Hemarthrosis
 Hematuria
Thrombosis and embolism
 oropharyngeal and central nervous system bleeding
 Predisposing risk factors for thrombosis
 atherosclerotic vascular disease
COMPARISON BETWEEN FACTOR 8 DEF AND VWF  porcine factor VIII concentrates, which may not be
affected by inhibitors
 prothrombin complex concentrates can bypass the
block in coagulation produced by the inhibitor
type II inhibitor
 have a low antibody titer that
 not stimulated by factor VIII infusion
 may respond to higher doses of factor VIII
 infusion of recombinant factor VIIa
 activates factor X directly and bypasses the
inhibitor-induced block

Inhibitors are identified by assay TESDA (ito yung pagkakarinig

LABORATORY TESTS ko char!) TESDA identifies patient whether he is a responder or
 prolonged PTT not. If non responder, no TESDA, give HIGH DOSE factor VIII. If
 other tests normal responder, give other forms of treatment but not factor 8.
 platelet count
 bleeding time GENETIC COUNSELLING AND EDUCATION
 PT  defective allele in some families by examining the
 specific assays for factor VIII inheritance of restriction fragment length
polymorphisms (RFLP) linked to the factor VIII gene
TREATMENT  specific mutation has been defined in the factor VIII
 factor VIII concentrates gene, it can be readily detected by gene amplification
 unit of factor VIII infused is the amount and allele-specific oligonucleotide hybridization
present in 1 mL normal plasma, will raise the  inversion arising from homologous recombination
plasma level of the recipient by 2%/kg of between sequences in intron 22 and an upstream
body weight gene
 main treatment for Hemophilia A  readily detected by polymerase chain
 in absence of this,we can replace it with FPP reaction (PCR) or Southern blotting
or cryoprecipitate  carriers of hemophilia usually produce sufficient
 desmopressin (DDAVP) factor VIII from the factor VIII allele on their normal X
 mild hemophilia chromosome for normal hemostasis
 transiently increases the factor VIII level
 Plasma products enriched in factor VIII HEMOPHILIA B/FACTOR 9 DEF
 FFP  Factor IX
 Cryoprecipitate  single-chain, 55-kDa proenzyme
 Disadvantage include inhibitor formation,  converted to an active protease (IXa) by
which is formation of antibodies against factor XIa or by the tissue factor-VIIa
factors complex
 Factor IXa then activates factor X in
COMPLICATIONS conjunction with activated factor VIII
 episodes of hepatitis  require vitamin K for biologic activity
 AIDS-related syndromes  Factor IX gene is on the X chromosome
 iron-deficiency anemia  Christmas disease
 mild Coombs-positive hemolytic anemia  1 in 100,000 male births
 inhibitors to factor VIII  indistinguishable clinically from factor VIII deficiency
 requires different treatment (only differs with
INHIBITORS TO FACTOR 8 treatment compared with hemophilia A)
Inhibitors to factor VIII  fresh-frozen plasma or a plasma fraction
 10 to 20% of patients enriched in the prothrombin complex
 usually IgG antibodies that rapidly neutralize factor proteins
VIII activity  Monoclonally purified or recombinant factor
 Two types of inhibitors are found with different IX preparations
biologic characteristics and different clinical  complications
presentations  hepatitis, chronic liver disease, and AIDS, the
type I inhibitors therapy of factor IX deficiency has a special
 typical anamnestic response hazard
 raise antibody titer following exposure to factor VIII
 FACTOR XI DEFICIENCY  acquired form of dysfibrinogenemia
 liver disease, hepatomas, AIDS, and
 Factor XI lymphoproliferative disorders
 160-kDa dimeric protein
 activated to an active protease (XIa) by FACTOR XIII DEFICIENCY AND DEFECTIVE FIBRIN CROSS-
factor XIIa, in conjunction with high- LINKING
molecular-weight kininogen and kallikrein  Factor XIII
 inherited as an autosomal recessive trait  transglutaminase that stabilizes fibrin clots
 common in Ashkenazi Jews by forming e-amino-g-glutamyl cross-links
 spontaneous bleeding is less between adjacent a and g chains of fibrin
 hemarthroses are rare  Factor XIII deficiency is an extremely rare inherited
 present with posttraumatic bleeding or with bleeding syndrome
in the perioperative period  manifestations
 menorrhagia  bleeding from their umbilical stump or
 tx:daily infusions of fresh-frozen plasma circumcision
 poor wound healing
OTHER FACTOR DEFICIENCIES  high incidence of infertility among males and
 Deficiencies in factors V, VII, X, and prothrombin  abortion among affected females
(factor II) are exceedingly rare autosomal recessive  intracerebral hemorrhage
disorders  single infusion of FFP or Fibrogammin is effective
 spontaneous or posttraumatic musculoskeletal  normal hemostasis requires only 1% of normal
bleeding or menorrhagia can occur enzyme activity
 hemarthroses are uncommon
 Fresh-frozen plasma is the appropriate therapy VITAMIN K DEFICIENCY
 Vitamin K
AFIBRINOGENEMIA AND DYSFIBRINOGENEMIA  fat-soluble vitamin
 Fibrinogen  Dietary vitamin K is absorbed in the small intestine
 340-kDa dimeric molecule and stored in the liver
 two sets of three covalently linked  also synthesized by endogenous bacterial flora in the
polypeptide chains small intestine and colon
 abundant plasma protein (2.5 g/L)  it is usually a multiple factor def
 thrombin sequentially cleaves fibrinopeptides A and B  deficiency causes include
from the Aa and Bß chains of fibrinogen to produce  antibiotic use
fibrin monomer, which then polymerizes to form a o due to suppression of the normal
fibrin clot flora to produce vit K
 needed for platelet aggregation and fibrin formation  hepatocellular diseases (alam nyo na to)
 severe deficiency does not usually cause serious  malabsorption, colitis, medications
bleeding except after surgery

Afibrinogenemia
 no detectable fibrinogen in plasma or platelets
 have infrequent, mild bleeding episodes
Dysfibrinogenemias
 mutations resulting to altered
 release of fibrinopeptides from the Aa and
Bß chains of fibrinogen
 rate of polymerization of fibrin monomers
 sites for fibrin cross-linking
 inherited as autosomal dominant traits Following absorption, vitamin K is converted to an active
 slightly prolonged PT and PTT, a prolonged thrombin epoxide in liver microsomes and serves as a cofactor in the
time, and a disparity in levels of fibrinogen measured enzymatic carboxylation of glutamic acid residues on
with functional and immunologic assays prothrombin complex proteins.Epoxide is the active form and
 most patients have no symptoms or only moderate is reduced back to vt K by a liver memb reductase. Warfarin
bleeding blocks the actio of reductase and competitively inhibits the
 few induce a hypercoagulable state and increase the effect of vit k.
risk of thrombosis,
 others have been associated with an increased Major causes of vitamin K deficiency
incidence of abortion  inadequate dietary intake
  intestinal malabsorption thrombogenic stimuli cause the deposition of
 loss of storage sites due to hepatocellular disease small thrombi and emboli throughout the
microvasculature
Neonatal vitamin K deficiency  hemorrhagic phase
 has disappeared with the routine administration of  procoagulant consumption and secondary
vitamin K to all newborn infants fibrinolysis
Acute vitamin K deficiency
 can become deficient within 7 to 10 days
 common in patients recovering from biliary tract
surgery who have no dietary intake of vitamin K, have
T-tube drainage of bile, and are on broad-spectrum
antibiotics
 biliary tract surgery can cause bile fluids to be
drained, so there will be poor absorption of Vit k
leading to hematomas and increased bleeding
tendencies
decrease plasma levels of all the prothrombin complex
proteins
 factors II, VII, IX, X DIC is initiated when there is tissue damage. There will be
 sya kasi yung responsible sa post translation ng release of toxins that will activate coagulation cascade and
factors na to activate the thrombolytic phase. It generates thrombin and
 clotting factors are activated by vit k causes fibrin deposition and thrombus formation in different
 Vit K epoxide reductase is used for recycling vit K. This blood vessel. Thrombosis in many organs result in multiple
is the enzyme inhibited by warfarin organ failure…. Awwwww 
 proteins C and S
 prolonged PT (emphasized by doc) and a normal PTT CLINICAL MANIFESTATION
 as the levels of the other factors fall PTT will also
become prolonged  extensive skin and mucous membrane bleeding and
Treatment hemorrhage from surgical incisions or venipuncture
 vitamin K 10mg parenterally adm or catheter sites
 rapidly restores vitamin K levels in the liver  peripheral acrocyanosis, thrombosis, and
 permits normal production of PT complex pregangrenous changes in digits, genitalia, and nose
proteins within 8 to 10 h  chronic DIC and malignancy
 first line of treatment, if patient has lab  laboratory abnormalities without any
results of prolong PT and PTT, you have to evidence of thrombosis or hemorrhage
give first Vit K and if there is improvement, it
means it is really vit K def, if hindi nag
improve then isip isip na tayo.Malamang di
yan vit K def, it could be due to another cause
like liver dse.
 FFP
 severe hemorrhage
 immediately corrects the hemostatic defect
 has all the clotting factors
 if patient is not in severe bleeding, we can  vascular obstruction as a consequence of thrombosis
just give parenteral vit K so that PT can but more often haemorrhage, as a result of
normalize after it after 10-12 hours consumption of platelets and coagulation factors, is
 monthly injections of vitamin K 10mg the dominant feature
 if cause cannot be eliminated

DISSEMINATED INTRAVASCULAR COAGULATION

 explosive and life-threatening bleeding disorder or a
relatively mild or subclinical disorder
 associated with obstetric catastrophes, metastatic
malignancy, massive trauma, and bacterial sepsis
 thrombotic phase
 showing bruising and bleeding into the soft tissues of immediate anticoagulation with intravenous
the arm heparin
 In many cases of DIC there is so much activation of  low-grade DIC
fibrinolysis that clinical features of thrombosis are  plasma and platelet replacement
absent  do not require heparin
 arm of a patient with disseminated intravascular  Chronic DIC
coagulation (DIC) showing haemorrhage  can be controlled with long-term heparin
 DIC was found to have been caused by abnormal infusion
clotting in association with a dissecting aortic
aneurysm COAGULATION DISORDERS IN LIVER DISEASE
Causes of hemorrhage in patients with liver disease
LABORATORY  due to an anatomic lesion that is exacerbated by a
 thrombocytopenia hemostatic defect
 presence of schistocytes or fragmented rbc that arise  complications of portal hypertension
from cell trapping and damage within fibrin thrombi  esophageal varices (can cause more
 prolonged PT and PTT and thrombin time bleeding)
 presence of clot can activate plasminogen to begin  gastritis and peptic ulcer disease
clot lysis. This will cause release of D-dimers and cause  splenomegaly
more bleeding  vitamin K deficiency
 reduced fibrinogen level from depletion of  Liver cannot store the vitamin
coagulation proteins  Cholestasis
 elevated fibrin degradation products (FDP) from  decreased production of other coagulation proteins
intense secondary fibrinolysis
 fibrinogen and factor V
 D dimer immunoassay, which measures
 antithrombin III , proteins C and S
cross-linked fibrin derivatives is a more
 clearance site for activated coagulation factors and
specific FDP assay
fibrinolytic enzymes

LABORATORY TESTS
Laboratory tests
 prolongation of the PT and PTT
 mild thrombocytopenia
 normal fibrinogen level
 severe thrombocytopenia or a low fibrinogen level
suggests the additional complication of DIC

TREATMENT
 fresh-frozen plasma
 safest replacement therapy for a patient
with liver disease
 supplies all known coagulation factors
 may precipitate hepatic encephalopathy and
cause fluid and sodium overload

FIBRINOLYTIC DEFECTS
TREATMENT
 a2 plasmin inhibitor deficiency or plasminogen
 an attempt to correct any reversible cause of DIC
activator inhibitor (PAI) 1
 measures to control the major symptom, either
 rapid fibrinolysis following fibrin deposition
bleeding or thrombosis
after trauma or surgery and may experience
 a prophylactic regimen to prevent recurrence in
recurrent hemorrhage
cases of chronic DIC
 cirrhosis
 bleeding as a major symptom
 impaired clearance of tissue plasminogen
 fresh-frozen plasma to replace depleted
activator (tPA) and systemic fibrinolysis that
clotting factors
may contribute to their hemorrhagic defect
 platelet concentrates to correct
 metastatic prostatic cancer
thrombocytopenia
 primary fibrinolysis
 acrocyanosis and incipient gangrene or other
Clues to the diagnosis
thrombotic problems
 low fibrinogen level
 normal PT and PTT
 normal or nearly normal platelet count
 primary fibrinolysis
 elevated titer of FDP but a normal D dimer level
 Patients with clearly established primary fibrinolysis
should not receive heparin
 require plasma therapy and, occasionally, fibrinolytic
inhibitors such as EACA
 EACA should not be given to patients suspected of
having DIC unless they are also receiving heparin,
since EACA can cause massive, often fatal, thrombosis
in a patient with DIC
CIRCULATING ANTICOAGULANTS
 Specific inhibitors
 inactivate individual coagulation proteins
and may cause severe hemorrhage
 15 to 20% of patients with factor VIII or
factor IX deficiency who have received
plasma infusions
 also occur in previously normal individuals
 most common target protein is factor VIII,
inhibitors with specificity for each of the
coagulation proteins occur
 Specific inhibitors anti-factor VIII antibodies
seen in
o hemophiliacs
o postpartum females
o patients on various drugs
o systemic lupus erythematosus (SLE)
patients
o normal elderly individuals
o AIDS
 Nonspecific (lupus-like) inhibitors
 prolong coagulation tests by binding to
phospholipids
 assayed by their anticoagulant effect [lupus
anticoagulant (LA) activity] or their ability to
bind to the complex phospholipid cardiolipin
[anticardiolipin antibody (ACLA) activity]
 patients with SLE
 patients with many other disorders
 normal individuals
 Laboratory feature
 failure of normal plasma to correct a
prolonged PT, PTT or both
 specific inhibitor
o progressively inactivate a IX, and X, may also reduce the concentration of
coagulation protein and thus
prolong whichever of these
screening tests requires the
participation of that clotting factor
persists after dilution
 Nonspecific inhibitors
o immediately prolong the PT and PTT
o low dilution, block multiple
coagulation reactions
o overcome by altering the quantity
or type of phospholipid or by
diluting the plasma
Treatment
 specific inhibitors
 activated prothrombin complex concentrates
to bypass the antibodies against factors VIII
or IX
 plasmapheresis or exchange transfusion to
lower antibody titer
 acquired factor VIII antibody
 Immunosuppressive
 Majority lose their antibody and recover
within 6 to 12 months
 acute mortality rate from bleeding may approach 10%
INHERITED THROMBOTIC DISORDERS
 clinical presentations
 strong family history of thrombosis
 episodes of recurrent venous
thromboembolism
 patients who develop venous
thromboembolism without a clear
predisposing factor
 symptoms by their early twenties
ANTITHROMBIN DEFICIENCY
 Plasma antithrombin III content is 5 to 15 mg/L (50 to
150%)
 antithrombin III concentration is measured by
immunoassay and the plasma antithrombin and
heparin cofactor activity assessed with functional
assays
 acute thrombosis or embolism can be treated with
intravenous heparin and oral anticoagulants for life to
prevent recurrent thrombosis
 Asymptomatic individuals should receive prophylactic
anticoagulation with heparin or plasma infusions to
raise their AT level before procedures that may
increase risk of thrombosis
DEFICIENCIES OF PROTEINS C AND S
 recurrent venous thrombosis and pulmonary
embolism
 Vit K lower the level of the procoagulant factors II, VII,
proteins C and S
 protein C-deficient may develop warfarin-induced
skin necrosis
 Patients with homozygous protein C deficiency
require periodic plasma infusions rather than oral
anticoagulants to prevent recurrent intravascular
coagulation and thrombosis
 Protein C is a vitamin K-dependent hepatic protein
that binds to the endothelial cell surface protein
thrombomodulin and is converted to an active
 protease by thrombin Activated protein C, in UFH forms change in
conjunction with protein S, proteolyzes factors Va and conformation in receiving
VIIIa, which shuts off fibrin formation. Activate protein loop to bind to
C may also stimulate fibrinolysis and accelerate clot antithrombin factor 9 and
lysis 10
LMW Heparin Short saccharide unit and
PROTHROMBIN GENE MUTATION lower weight, same with
 a specific point mutation in the prothrombin gene function of UFH only it just
[conversion of G to A at position 20210 (G20210A)] binds with factor 10 (aba
predisposes to venous thrombosis and embolism aba, ito ang loyal isa lang
 inheritance of multiple mutations increases the risk of ang kinakabitan lols)
thrombosis Fondaparinoux Enhances factor 10
inhibition
TREATMENT FOR ALL INHERITED THROMBOTIC
DISORDERS


standard initial therapy with heparin
followed by 3 months of oral warfarin
GOOD LUCK SA FINALS
 Antithrombin III deficiency who become symptomatic
 high likelihood of recurrent events and
GUYS!!!!!

should be placed on lifelong anticoagulation
Protein C or S deficiency or factor V Leiden and
TIIS GANDA/POGI MUNA TAYO
PTG20210A patients SA PUYAT!
 lower likelihood of recurrent disease
 Long-term anticoagulation for second or TANDAAN,SURG BLOCK NA

subsequent episode of thromboembolism
Patients who present with DVT or pulmonary NEXT SEM   
embolism during pregnancy or while using oral
contraceptives have a 30% chance of having factor V


Leiden
3 months of oral warfarin
Xoxo, Istepania <3 <3
 allow maximal healing and reendothelialization of the
thrombosed vessels and minimize recurrence in the
damaged vascular beds

ANTITHROMBOTIC TREATMENTS
This is not on doctora’s ppt but she mentioned it in the
lecture so here it is..

Aspirin Irreversible
COX 1 inhibitor
Inhibitor of thromboxane
Can be given in disorders of
primary and secondary
hemostasis
SE: bleeding (dugo dugo!!!)
NSAID Inhibit COX
reversible
GP2b3a antagonist Inhibit the one that binds to
fibrinogen
ANTIPLATELETS
clodipogrel Inhibits ADP which is a
potent platelet aggregator
ANTICOAGULANTS
UF Heparin Longer saccharide unit and
binds to antithrombin,
enhancing antithrombin
activity -> antitrombin +