Bruising And Bleeding Flashcards
Major causes of bleeding disorders
. Structural
. Platelet-related
. Clotting factor-related (platelet plug not stable)
Leukemia
. Group of neoplasticism disorders affecting leukopoietic tissues in body
. Characterized by leukocytosis, immature leukocytes in peripheral blood
. Proliferation of immature cells in marrow suppressing normal cell growth (like MK cells)
Idiopathic thrombocytopenic purpura
. Platelet destruction inc. from circulating antiplatelet antibodies in plasma
. Platelet survival is shortened
Hemophilia A/B
. Genetic defect x-linked recessive
. Inc. bleeding from clotting disturbance
. 70% people are inherited, others from spontaneous mutation
. A is deficiency in factor VIII, b from IX deficiency
Disseminated intramuscular coagulopathy
. Systemic activation of blood coag resulting in generation and deposition of fibrin
. Leads to microvascular thrombi in organs causing dysfunction
. Possible consumption and subsequence exhaustion of coag proteins and platelets may cause severe bleeding
Diascopy
. Test for blanchability by applying pressure w/ finger and observing color change
Normal platelet count
. 150,000-400,000
. Thrombocytopenic: less than 150,000
. Thrombocytosis: over 400,000
Partial thromboplastin time
.blood test evaluating integrity of intrinsic and common coag pathway and to monitor patients on Heparin
. Normal 25-37 s.
Prothrombin time
. Blood test that measures how quickly blood clots
. Normal 10-14 s.
International normalized ratio (INR)
. 1.1 or below is normal
. 2-3 is therapeutic range when taking blood thinners
Bleeding time (BT)
. Standard filter paper should be every 30 s. Until blood completely stops
. Normal: 2-9 minutes
. Risk of bleeding inc. w/ time over 10 min.
Unexplained nosebleeds suggest ___
. Platelet defects
5 causes of dec. platelet production
. Meds . Bone marrow replacement by malignancy, fibrosis, or granulomas . Bone marrow aplasia . Alcohol . B12 deficiency
5 causes of inc. platelet consumption
. Splenic sequestration . Autoimmune thrombocytopenia (idiopathic, HIV, lupus, lymphoproliferative issues, meds) . Disseminated intravascular coag. . Thrombotic thrombocytopenic pupura . Sepsis
Evaluation of bleeding patient
. Clinical context (post-surgical, sepsis, exposure to anticoags)
. Personal history (onset in infancy = heritable condition, as adults = milder heritable condition or acquired cause)
. Family history
. Location (mucocutaneous bleeding = suggests qualitative/quantitative platelet defects, joint/soft tissue= disorders of coag factors
Platelets
. Critical role in hemostasis
. Functions: adhesion, activation, aggregation
Bernard-soulier syndrome
. Deficiency in GpIb platelet Factor
Glanzmann thrombasthenia
. Deficiency in GpIIb-IIIa complex in platelet clotting
Von willebrand Disease
. Most common inherited bleeding disorder, most cases autosomal dominant
. Due to issues w/ Von willebrand factor (glycoprotein that binds platelets to subendothelium and is a carrier of factor VIII)
Type I Von willebrand disease
. Type i: 75-80% pts, mild to moderate bleeding, don’t bleed spontaneously, involves skin and mucous membranes
. Keep in mind for teen patients
. Normally diagnosed when excessive bleeding occurs after procedure, heavy or long menstrual bleeding (changing of pad once an hour)
Type II Von willebrand disease
. 15-20% patients
. Moderate to severe bleeding
. Usually present in childhood or adolescence
Type 3 Von willebrand disease
. Severe bleeding in infancy and childhood
. Autosomal recessive inheritance
Bernard-Soulier syndrome
. Autosomal recessive inheritance
. Reduced or abnormal platelet membrane expression of GIb/IX
. Failure of adhesion
. Severity of symptoms vary
. Clinical features: petechia, ecchymosis, recurrent epistaxis
Glanszmann’s thrombasthenia
. Autosomal recessive
. Platelets contain low or defective glycoprotein GpIIb/IIa (fibrinogen receptor)
. Platelets aggregation impaired os no thrombus formation
. Clinical features: petechia, ecchymosis, recurrent epistaxis
Idiopathic thrombocytopenia
. Acquired disorder
. Immune mediated destruction of platelets (antibodies against. Platelet membrane antigens)
. Only bleeding presentation, spontaneous bruising doesn’t occur until platelet count is under 30,000
. Fatigue common
. Diagnosis of exclusion
. Secondary causes: leukemia, meds, lupus, cirrhosis, HIV, hep C
ITP in children
. Acute
. Follow after viral vaccines
. Resolves w/in a few weeks w/o treatment
ITP in adults
. Chronic . No prodrome . Idiopathic . Affects more women . Requires treatment
Disseminated intravascular coagulation
. Always has underlying etiology
. Cause must be identified to treat coagulopathy triggering factor damages vessels
. Uncontrolled activation of coag cascade where many clots develop throughout vasculature
. Inc. clotting depletes platelets and clotting factors creating excessive bleeding
. May cause tissue ischemia from occlusive thrombi AND bleeding from consumption of platelets and clotting factors
. Caused from sepsis, trauma, burns, obstetric complications, and cancer
. Bleeding in multiple sites, petechia/ecchymosis, gangrene
Drug induced thrombocytopenia
. Severe mucocutaneous bleeding 7-14 days after exposure
. Discontinuation of meds leads to resolution in 7-10 days
. Recovery kinetics depends on rate of drug clearance
Heparin-induced thrombocytopenia
. Immunologically mediated adverse reaction causing formation of IgG antibodies to heparin-platelet factor 4 complexes
. Causes inappropriate activation of platelets, thrombocytopenia, and pro thrombi state
. Thrombosis in both arterial and venous systems occur in up to 50% of cases
. Decline in baseline platelet count of 50% or more
. Onset occurs w/in 5 to 14 days or exposure to heparin
Aspirin
. Irreversibly binds to platelets
. Inhibits COX and TBA2 production
. Produces inhibitory effect of platelet aggregation
NSAIDS
. Inhibits platelet COX and TXA2
. Reversible bind to platelets for limited time
Plavix
. Platelet receptor inhibitor
. Inhibits platelet adhesion and aggregation
Alcohol effect on platelets
. Dec. TXA2 release
Hemophilia
A: VIII issue
. B: IX issue
. Severity inversely proportional to factor levels
. Mild: spontaneous bleeding rare but can occur w/ significant surgery or trauma
. Severe: presents in infants w/ spontaneous bleeding into joints
. Female carries asymptomatic
Hemophilia C
. Factor XI deficiency
. Autosomal recessive
. Jew problem
. Most mild form of bleeding
Factor XIII deficiency
. Involved w/ process of cross linking fibrin
. Delayedbleeding occurs hours to days after hemostatic challenge
. Spontaneous intracranial hemorrhage and recurrent pregnancy loss are indicators
Acquired antibodies to factor VIII
. Acquired hemophilia A
. Spontaneous antibodies to factor VII in adults w/o prior history
. High risk: lymph malignancy, CT disease, post party’s, or post surgery
. Clinical presentation: soft tissue ecchymosis, hematoma, mucosal bleeding
. Leads to severe life threatening bleeding
Liver disease effect on bleeding
.dec. synthesis of clotting factors
. Splenomegaly
. Thrombopoietin controls circulating platelets by stimulating marrow to produce megakaryocytes and is impaired
. Complication from cirrhosis may be esophageal varices
Vit, K deficiency
. Dec. synthesis of factors II, VII, IX,
. Occurs as result of dietary deficiency, malabsorption, dec. production by intestinal bacteria
Warfarin (Coumadin)
. Vit. K antagonist
. Inhibits vit. K dependent carboxylase important for coag factors II, VII, IX, and X
