HEMORRHAGIC DIATHESIS
HEMORRHAGIC DIATHESIS IS A DISEASE, CHARACTERIZED BY EXCESSIVE BLEEDING. ACCORDING TO PATHOGENESIS, IT IS CLASSIFIED INTO COAGULOPATHY, PLATELET DISORDER (THROMBOCYTOPENIA AND THROMBOCYTOPATHY) AND VASOPATHY. EACH TYPE IS SUBDIVIDED INTO CONGENITAL AND ACQUIRED.
Petechial-ecchymosis
Hematoma
Mixed (Petechia & Hematoma)
Vasculatic
Angiomatosic
The main bleeding types
THE MAIN BLEEDING SICKNESS TYPES• Hematomic (massive, deep, painful; bleeding may occur anywhere. The most
common sites of bleeding are into joints (knees, ankles, elbows), into muscles, from the gastrointestinal tract, cause of the bleeding can be intramuscular injection; characterized by early postoperative & posttraumatic bleeding)
• hematoma
• petechia-spotted (macula)
MACULA-HEMATOMA
VASCULITIC PURPURA
ANGIOMA
THE MAIN COAGULOGRAM INDEXES11 IndexIndex HypoHypo
coagulationcoagulationNormoNormo
coagulationcoagulationHyperHyper
coagulationcoagulation
Bleeding time (by Lee-Bleeding time (by Lee-White methods), minWhite methods), min
>>55 5-35-3 << 33
Platelets numberPlatelets number <<180180 180-320180-320 >>320320
Platelet adhesivenessPlatelet adhesiveness <<2323 23-4423-44 >>4545
Time of plasma Time of plasma recalcification, secrecalcification, sec
>>120120 120-60120-60 <<6060
Heparin tolerance test, Heparin tolerance test, minmin
>>1111 11-811-8 <<88
Prothrombin index, %Prothrombin index, % <<8080 80-10080-100 >>100100
U-factorU-factor <<8080 80-10080-100 >>100100
Procorventin (VII Procorventin (VII factor), %factor), %
<<8080 80-10080-100 >>100100
Fibrinogen, g/lFibrinogen, g/l <<22 2-42-4 >>44
SCREENING TESTS FOR BLEEDING DISORDERS
TestTest Abnormality detectedAbnormality detectedBlood count and filmBlood count and film Anaemia, leukaemia, Anaemia, leukaemia,
disseminateddisseminatedintravascular coagulationintravascular coagulation
Platelet countPlatelet count ThrombocytopeniaThrombocytopeniaActivated partial thromboplastin Activated partial thromboplastin timetime
Deficiency of all coagulation Deficiency of all coagulation factorsfactorsexcept VII, especially follows VIII except VII, especially follows VIII and IX;and IX;heparinheparin
Prothrombin timeProthrombin time Deficiency of factors I, II, V, VII, Deficiency of factors I, II, V, VII, and X;and X;warfarinwarfarin
Thrombin time or fibrinogenThrombin time or fibrinogen Hypofibrinogenaemia or Hypofibrinogenaemia or dysfibrinogenaemia; heparin; dysfibrinogenaemia; heparin; fibrin degradation productsfibrin degradation products
Bleeding time Bleeding time Test of platelet-vessel wall Test of platelet-vessel wall interactioninteraction
COAGULOPATHY
•I. Congenital• Deficiency of coagulation factor VIII (hemophilia A)• Deficiency of coagulation factor IX (hemophilia B)• Deficiency of coagulation factor XI (hemophilia C)• Deficiency of other coagulation factors (I, II, V, VII, IX, X and XIII) • Deficiency of XII factor, prekallikrein or kininogen, protein C and S (without excessive bleeding)• von Willebrand’s disease (angiohemophilia)
COAGULOPATHY• II. Acquired• 1) Hypoprothrombinemia• • Deficiency of vitamin K due to acholia of GIT (in
cholestatic jaundice)• In overdose of indirect anticoagulant (antagonist of vitamin K)• In liver cirrhosis (due to reduced protein production)
• 2) Consumption of coagulation factors (II stage of DIC)• 3) Heparin overdose • 4) Activation of fibrinolytic system• • In administration of streptokinase etc.
• In trauma, obstetrical or surgical operations• In malignant neoplasms• In shock, sepsis, hematological malignancies, III stage of DIC
PLATELET DISORDERS
•Thrombocytopathy•I. Congenital (deficiency of platelet membrane glycoprotein) – Glanzmann's Thrombasthenia•II. Acquired (normal platelet count in blood and bone marrow but its functions are decreased)•• Drugs (after intake of antiplatelet agents: aspirin, Ticlide®);• Immune, toxic, septic processes;• Hematological malignancies and anemias•Thrombocytopenia (decrease in the number of platelets)•I. Werlhof’s disease - autoimmune thrombocytopenic purpura•II. Symptomatic•• Immune (heteroimmune, isoimmune,) • Toxic (in phosphorus poisoning etc.)• Methaplastic (in hematological malignancies or myelocarcinosis)• Drug-induced (cytostatics)
THROMBOCYTOPENIAo Thrombocytopenia (decrease in the number of
platelets) o - Idiopathic thrombocytopenic purpura (ITP) o - Thombotic thrombocytopenic purpura (TTP) o - Heparin-induced thrombocytopenia (HIT)o - Hemolytic-Uremic Syndromeo - Chronic liver disease
VASOPATHY
• I. Congenital
• • Telangiectasiae (Rendu-Osler-Weber disease)• Aneurysm of fine vessels • Ehlers-Danlos syndrome, Marfan’s syndrome, retinocerebral angiomatosis (von Hippel-Lindau syndrome), encephalotrigeminal angiomatosis (Sturge-Kalisher-Weber syndrome)
• II. Acquired
• • Hemorrhagic vasculitis – Henoch-Schönlein purpura• Immune vasculitis• Systemic vasculitis• Avitaminosis of vitamin C
THE CLOTTING MECHANISM
INTRINSIC EXTRINSIC
PROTHROMBIN THROMBIN
FIBRINOGEN
FIBRIN(II) (III)
(I)V
X
Tissue Thromboplastin
Collagen
VII
XII
XI
IXVIII
COAGULATION PATHWAY• Two pathways for fibrin clot formation:
• Intrinsic• Initiated by negatively charged surface
• Extrinsic• Initiated on tissue injury
• Both pathways converge on a final common pathway
• Prothrombin Thrombin (Most critical step )• Fibrinogen Fibrin Clot
• The pathways are complex and involve many different proteins (called blood clotting factors)
COAGULATION CASCADE - CONTINUED
Control of coagulation
• Antithrombins (e.g., antithrombin III)
• Proteins C and S
• Fibrinolytic cascade
• Plasminogen plasmin fibrin break down products (*FDP or FSP) – d-dimer is most important of the FDPs
*FDP / FSP – Fibrin degradation products / Fibrin split products
Bleeding disorders
Vascular abnormalities
Platelet disordersClotting factorabnormalities
DIC
CLOTTING FACTOR ABNORMALITIES
• Congenital disordersCongenital disorders• Von Willebrand disease –MC with minimal bleedingVon Willebrand disease –MC with minimal bleeding• Factor VIII Deficiency - Hemophilia A or Classic TypeFactor VIII Deficiency - Hemophilia A or Classic Type• Factor IX Deficiency – Hemophilia BFactor IX Deficiency – Hemophilia B
• Acquired disordersAcquired disorders• Vit. K deficiency Vit. K deficiency • Oral anti-coagulantsOral anti-coagulants
• Coumarin derivativesCoumarin derivatives = warfarin – inhibit Vit. K = warfarin – inhibit Vit. K factors factors
• Liver diseases ↓ synthesis of factorsLiver diseases ↓ synthesis of factors
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factor IX deficiency
factor VIII deficiency
factor XI deficiency
А В С
Haemophilia
FORMS Haemophilia A - factor VIII deficiency, "classic
haemophilia" (X-linked) Haemophilia B - factor IX deficiency, "Christmas
disease" (X-linked) Haemophilia C - factor XI deficiency (Ashkenazi
Jews, autosomal recessive) The unrelated type 1 and type 2
von Willebrand disease (vWD)
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Mild form
1 2
F VIII C level 1-5 %
Moderate form
3
F VIII C level less than 1 %
Severe form
F VIII C level 5-25 %
Classification (F VIII C level)
CLINICAL SEVERITY OF HAEMOPHILIA A AND B
Factor value*Factor value* Bleeding tendencyBleeding tendency
Less than 0.02Less than 0.02 Severe - frequent spontaneous bleeding Severe - frequent spontaneous bleeding into joints, muscles, and internal organsinto joints, muscles, and internal organs
0.02-0.050.02-0.05 Moderate—some “spontaneous” Moderate—some “spontaneous” bleeds,bleeds,bleeding after minor traumableeding after minor trauma
More than More than 0.050.05 Mild—bleeding only after significant Mild—bleeding only after significant trauma ortrauma orsurgerysurgery
* Normal value of factors VIII and IX is 0.5-1.5* Normal value of factors VIII and IX is 0.5-1.5
HEMOPHILIA AHEMOPHILIA A• MC hereditary disease with serious bleeding
• X-linked recessive• In 30% No family history (new mutations)• 15% of severe cases develop factor VIII inhibitors
• ↓ amount or activity of factor VIII• factor VIII = cofactor for activation of factor X in the
coagulation cascade• Symptoms usually – hemoarthrosis, bruising,
hemorrhage after trauma or surgery
SIGNS & SYMPTOMS •
Symptoms of hemophilia are usually first noticed during infancy or childhood. However, some people with milder forms of hemophilia may not develop symptoms until later on.
The following are signs of hemophilia that may be noticed shortly after birth: Bleeding into the muscle, resulting in a deep bruise after receiving a routine vitamin K shot.
Prolonged bleeding after a male child is circumcised. •
Other symptoms of hemophilia include: Bleeding into a joint or muscle that causes pain and swelling. Abnormal bleeding after an injury. Easy bruising. Frequent nosebleeds. Blood in the urine (hematuria).
• The most common bleeding problem a person with severe hemophilia has is bleeding into a joint (hemarthrosis), often without an injury.
Arhtropathy
Hematomic bleeding sickness types
Diagnostic criteria
Hemophilia
BIOCHEMICAL ASPECTS:
• Factor VIII circulates in the plasma as a complex of factor VIII and von Willebrand factor. The molecular weight of human factor VIII has been estimated to be 285,000. Hemophelia A in which factor VIII (antihemophelic factor) is either absent or dysfunctional is transmitted by X chromosomal inheritance. Hemophelia A is at least four times more common than hemophelia B.
DIAGNOSTIC CRITERIA
• Family_history_of_coagulation_disorders: positive APTT:abnormal
• Mixing_APTT:corrected Factor_VIII:C_activity:abnormal
Condition Prothrombin time
Partial thromboplastin time
Bleeding time Platelet count
Vitamin K deficiency or warfarin
prolongednormal or mildly prolonged
unaffected unaffected
Disseminated intravascular coagulation
prolonged prolonged prolonged decreased
von Willebrand disease
unaffected prolonged prolonged unaffected
Hemophilia unaffected prolonged unaffected unaffectedAspirin unaffected unaffected prolonged unaffectedThrombocytopenia
unaffected unaffected prolonged decreased
Uremia unaffected unaffected prolonged unaffectedGlanzmann's thrombasthenia
unaffected unaffected prolonged unaffected
Bernard-Soulier syndrome
unaffected unaffected prolongeddecreased or unaffected
TREATMENT
• In mild bleeding: 1-desamino-8-D-arginine vasopressin (DDAVP). The level of factor VIII must be maintained at least 30%.
• In non-life-threatening bleeding or pre-op: factor VIII concentrates. The minimal hemostatic level of factor VIII:C in this case is 50%.
• Central nervous system hemorrhage and severe bleeding: factor VIII concentrates. The level of factor VIII:C must be maintained at 80% - 100%.
• Each unit of factor VIII concentrates will raise the level of factor VIII by 2%/kg of body weight.
• Adjunctive therapy in dental surgery for mild and moderate hemophelia A: epsilon-aminocaproic acid (EACA).
• Avoidance of aspirin-containing compounds. • For monitoring therapy, factor VIII assay is the test of choice. • Dosage: the (activity ) units of factor VIII required can be calculated
from: 40*BW*(desired factor level-actual factor level)/100 • where BW is body weight in kg
TREATMENT
• The dose of factor VIII concentrate is calculated assuming that one unit of factor VIII is the amount present in 1 mL of plasma. Plasma volume is 40 mL/kg, and the volume of distribution of factor VIII:C is 1.5 times the plasma volume. Thus, to raise the level 100%, the dose should be 40 x 1.5 = 60 units/kg, or approximately 4000 units for a 70-kg individual. To raise the levels to 25% would require 1000 units. The half-life of factor VIII:C is approximately 12 hours. Thus, during major surgery, to achieve an initial level of 100% and maintain it continuously at greater than 50%, a dose of 60 units/kg (approximately 4000 units) initially followed by 30 units/kg (approximately 2000 units) every 12 hours should be adequate. During surgery, initially verify that these doses give the anticipated factor VIII levels. If factor VIII levels fail to rise as expected, an inhibitor should be suspected.
HEMOPHILIA BHEMOPHILIA B
• DEFICIENCY OF FACTOR IX• Factor IX deficiencyFactor IX deficiency• X-linked recessiveX-linked recessive• Much less commonMuch less common• Clinically= Clinically= indistinguishableindistinguishable from Hemophilia A from Hemophilia A
with with Similar lab findingsSimilar lab findings• Diagnosis by factor IX levelsDiagnosis by factor IX levels• Treat with recombinant IXTreat with recombinant IX
DIAGNOSTIC CRITERIA
• Family_history_of_coagulation_disorders:positive
• Mixing_APTT:corrected
• Factor_IX_assay:abnormal
• APTT:abnormal
TREATMENT
• For patients with mild form of factor IX deficiency with non-life-threatening bleeding, the treatment of choice is FFP. For the severe form of hemophelia B or in life- threatening situation, prothrombin complex concentrates are the treatment of choice.
TREATMENT
• Target levels of factor IX for therapy: Severe hemorrhage: 20% - 50% for 3-5 days, then 10% - 20% for the next 10 days.
• Minor hemorrhage: 20% for 7 days.
• Surgery: 50% - 70% for 2 days, then 30% - 40% for 3 days, then 20% for 7 days.
TREATMENT
• Dosage: the (activity) units of factor IX required can be calculated from: 80*BW*(desired factor level-actual factor level)/100
• where BW is body weight in kg
• Note that in-vivo recovery of factor IX is about 50%.
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15-20 UN/kg
1 2
Moderate
35-40 UN/kg
3
Severe.
70 UN/kg
Mild
Hemophilia A Treatment (cryoprecipitate)
VON WILLEBRAND'S DISEASE
Essentials of Diagnosis
• Family history with autosomal dominant pattern of inheritance.
• Prolonged bleeding time, either at baseline or after challenge with aspirin.
• Reduced levels of factor VIII antigen or ristocetin cofactor.
• Reduced levels of factor VIII coagulant activity in some patients.
Symptoms and Signs
• von Willebrand's disease is a common disorder affecting both men and women. Most cases are mild. Most bleeding is mucosal (epistaxis, gingival bleeding, menorrhagia), but gastrointestinal bleeding may occur. In most cases, incisional bleeding occurs after surgery or dental extractions. von Willebrand's disease is rarely as severe as hemophilia, and spontaneous hemarthroses do not occur (except in the rare type III). The bleeding tendency is exacerbated by aspirin. Characteristically, bleeding decreases during pregnancy or estrogen use.
THE MAIN BLEEDING SICKNESS TYPES• Mixed (Petechial & Hematomic) (combined
features of both types, but there are some difference: in contrast to hematomic - bleeding are into joints very rare, mostly it is located in subcutaneous, retroperitoneal, mesenteric, subserous intestinal layer or into internal organ);in contrast to petechial-ecchymosic bleeding - hemorrhagic syndrome characterized by large bruise)
TREATMENT• The bleeding disorder is characteristically mild, and no treatment is
routinely given other than avoidance of aspirin. However, patients often need to be prepared for surgical or dental procedures. The bleeding time is probably the best indicator of the likelihood of bleeding, and prophylactic therapy may be reasonably withheld if the procedure is minor and the bleeding time is normal.
• Desmopressin acetate (DDAVP) is useful for mild type I von Willebrand's disease and should be considered first. The dose is 0.3 mcg/kg, after which vWF levels usually rise two- to threefold in 30–90 minutes. It can also be given as a nasal spray; levels peak 2 hours after use.
• The antifibrinolytic agent aminocaproic acid (EACA) is useful as adjunctive therapy during dental procedures.
PLATELET HEMOSTATIC ACTIVITY
• 1. Pl stimulate vasoconstriction of injured vessels
• 2. Pl form hemostatic plug (platelet adhesion) + platelet aggregation to seal small vessel wall
• 3. Pl play role in fibrin clot formation
Bleeding disorders
Vascular abnormalities
***Platelet disorders
Clotting factorabnormalities
DIC
Bleeding disorders
Platelet disorders
↓production ↑destruction
SequestrationHypersplenism
Primary/IdiopathicITP
Acute/Chronic
SecondaryDrugs, HIV
THROMBOCYTOPENIA• Thrombocytopenia (or -paenia, or thrombopenia in short) is the
presence of relatively few platelets in blood.
• Generally speaking a normal platelet count ranges from 180,000 and 320,000 per mm3.
• Signs and symptoms
• Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count. Occasionally, there may be bruising, nosebleeds and/or bleeding gums.
• It is vital that a full medical history is elicited, to ensure the low platelet count is not due to a secondary process. It is also important to ensure that the other blood cell types red blood cells, and white blood cells, are not also suppressed.
THROMBOCYTOPENIA
Petechial-ecchymosic
Diagnostic criteria
1. Deacrease of platelets
PLATELET DISORDERSPLATELET DISORDERS
• Thrombocytopenia = Reduced platelet number
• Causes
• Decreased production of platelets
• vitamin B12 or folic acid deficiency
• Decreased platelet survival
• Immunologic or Nonimmunologic etiology
• Sequestration- Hypersplenism
• ameliorated by splenectomy
• Dilutional
• Massive transfusions
IMMUNE THROMBOCYTOPENIC PURPURA (ITP) • Cause
• Antiplatelet antibodies • Antigen - platelet membrane glycoprotein complexes
IIb-IIIa and Ib-IX• Morphology
• Peripheral Blood• thrombocytopenia, abnormally large platelets
(megathrombocytes or Giant platelets),• Marrow
• Normal or Increased magakaryocyte #• Diagnosis - by exclusion
• Bleeding time - prolonged, but PT & PTT - normal
↓ Marrow magakaryocyte # - your Diagnosis of ITP is ?????
NECESSARY EVALUATION
• • History: Isolated bleeding symptoms consistent with
thrombocytopenia without constitutional symptoms
(e.g. significant weight loss, bone pain, night sweats).
• • Physical examination: Bleeding symptoms in the absence of hepatosplenomegaly, lymphadenopathy, or stigmata of congenital conditions.
NECESSARY EVALUATION
• • Complete blood count: Isolated thrombocytopenia (platelet count <100 x 109/L). Anemia only if due to significant bleeding—otherwise normal red cell indices, white blood cell count and differential.
• • Peripheral blood smear: Identified platelets should be normal to large in size. Red and white blood cell morphology should be normal.
BONE MARROW EVALUATION• • Bone marrow examination is unnecessary in patients with the
typical features of ITP outlined above, irrespective of the age of the patient.
• • Bone marrow examination is felt to be unnecessary in children with typical ITP prior to initiation of treatment with corticosteroids, prior to splenectomy, or in patients who fail intravenous immunoglobulin (IVIg) therapy.
BONE MARROW EVALUATION• • The presence of abnormalities in the history, physical
examination, or the complete blood count and peripheral blood smear should be further investigated, e.g. with a bone marrow examination or other appropriate investigations, before the diagnosis of ITP is made.
ADDITIONAL EVALUATIONS
• • All adult patients with newly diagnosed ITP should undergo testing for HIV and HCV.
• • There is insufficient evidence to support the routine use of anti-platelet, antiphospholipid, and anti-nuclear antibodies, thrombopoietin levels, or platelet parameters obtained on automated analyzers in the evaluation of patients with suspected ITP.
DIAGNOSTIC CRITERIA:
• Plt_count:abnormal (low)
• Peripheral blood smear:no increase in schistocytes
• Bone_marrow:megakaryocytosis
THE MAIN BLEEDING SICKNESS TYPES• Petechia-ecchymosis (is usually localized to superficial sites such
as the skin and mucous membranes, wich often combined with menorrhagia, nose bleeding, gumms bleeding; rare – with gastrointestinal bleeding or brain hemorrhage; it is small, painless, provoked by simple action like skin cleaning, measure of blood pressure etc; pinch test is positive)
ITP
FeatureFeature AcuteAcute ChronicChronic
Age / SexAge / Sex ChildrenChildren Adult/FemaleAdult/Female
OnsetOnset AbruptAbrupt GradualGradual
Predisposing Predisposing FactorsFactors
Viral infection/ Viral infection/ vaccinevaccine
--
DurationDuration <2 months<2 months >6mnoths>6mnoths
PathogenesisPathogenesis -- IgG against Platelet IgG against Platelet GPGP
Peripheral Peripheral smearsmear
Thrombocytopenia & Thrombocytopenia & Giant PLTSGiant PLTS
SameSame
Bone marrowBone marrow Normal or Normal or ↑Megakaryocytes↑Megakaryocytes
SameSame
ITP
FeatureFeature AcuteAcute ChronicChronic
TestsTests Prolonged BT Prolonged BT & Normal PT & & Normal PT & PTTPTT
SameSame
Complication Complication (most (most dangerous)dangerous)
Intracranial Intracranial bleedbleed
SameSame
Clinical courseClinical course Spontaneous Spontaneous remissionremission
NoNo
TreatmentTreatment PLT. PLT. TransfusionTransfusion SplenectomySplenectomy
If <20,000If <20,000
NoNoIf <50,000If <50,000
Yes (refractory Yes (refractory cases)cases)
ConditionProthrombin time
Partial thromboplastin time
Bleeding time Platelet count
Vitamin K deficiency or warfarin
prolongednormal or mildly prolonged
unaffected unaffected
Disseminated intravascular coagulation
prolonged prolonged prolonged decreased
von Willebrand disease unaffected prolonged prolonged unaffected
Hemophilia unaffected prolonged unaffected unaffected
Aspirin unaffected unaffected prolonged unaffected
Thrombocytopenia
unaffected unaffected prolonged decreased
Uremia unaffected unaffected prolonged unaffectedGlanzmann's thrombasthenia
unaffected unaffected prolonged unaffected
Bernard-Soulier syndrome
unaffected unaffected prolongeddecreased or unaffected
MANAGEMENTOF ITP• The goal of all treatment strategies for ITP is to achieve a platelet
count that is associated with adequate hemostasis, rather than a normal platelet count. The decision to treat should involve a discussion with the patient and consideration of the severity of bleeding, anticipated surgical procedures, medication side effects, and health-related quality of life.
INITIAL MANAGEMENT OF ITP• Assessment of Disease Status:
• • What bleeding is the patient experiencing?
• • Determine the timing, location, and severity of
• bleeding symptoms.
• • Does this patient have any additional risk factors for bleeding such as use of antithrombotic agents or high-risk occupation?
• • Is a surgical procedure anticipated?
• • Is this patient likely to comply with recommended treatments?
• • Is the bleeding experienced by this patient interfering with his or her daily activities or causing significant anxiety?
GENERAL CONSIDERATIONS FOR INITIAL MANAGEMENT
• • The majority of patients with no bleeding or mild bleeding (defined here as skin manifestations only, such as petechiae and bruising) can be treated with observation alone regardless of platelet count.
• • First-line treatment includes observation, corticosteroids, IVIg, or anti-D immunoglobulin (anti-D).
• • Anti-D should be used with caution given recent FDA warnings of severe hemolysis. It is therefore not advised in patients with bleeding causing a decline in hemoglobin, or those with evidence of autoimmune hemolysis.
DRUG INDUCED THROMBOCYTOPENIAHEPARIN INDUCED THROMBOCYTOPENIA (HIT)
• Seen in 3-5% of patients treated with unfractionated heparin
thrombocytopenic after 1-2 weeks of Rx
• Caused by IgG antibodies against platelet factor 4/heparin complexes on platelet surfaces
• Exacerbates thrombosis, both arterial and venous (in setting of severe thrombocytopenia)
• Antibody binding results in platelet activation and aggregation.
• Rx - cessation of heparin
Other drugs???
PLATELET FUNCTIONAL DISORDERSPLATELET FUNCTIONAL DISORDERS
Bleeding disorders
Vascular abnormalities
Platelet disordersClotting factorabnormalities
DIC
VASCULAR ABNORMALITIESVASCULAR ABNORMALITIES• Causes
• Infections• Meningococcemia, Rickettsioses , Infective endocarditis
• Drug reactions
• Hereditary hemorrhagic telangiectasia• Autosomal dominant
• Cushing syndrome
• Henoch - Schönlein Purpura • systemic hypersensitivity disease of unknown cause
• polyarthralgia, and acute Glomerulonephritis
• Palpable purpuric rash, colicky abdominal pain
• Scurvy and the Ehlers-Danlos syndrome
• Amyloid infiltration of blood vessels
THE MAIN BLEEDING SICKNESS TYPES
• Vasculatic (hemorrhage due to inflammatory changes of small vessels, the main cause are immune disorders
or infectious agent)
THE MAIN BLEEDING SICKNESS TYPES• Angiomatosic (hemorrhage due to vascular dysplasia,
teleangiectasia; the main clinical criteria is relapsing bleeding without hemorrhage in skin, subcutaneous and other tissue; nose bleeding are most often, dangerous and massive)
Bleeding disorders
Vascular abnormalities
Platelet disordersClotting factorabnormalities
DIC
Thank you for attention!
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