Lecture: Platelet and Hemostatic Disorder Flashcards by Tristan Buenvenida

Assess the amount of platelets

Quantitative

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Defective platelet adhesion, secretion and aggregation

Qualitative

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Caused by clonal proliferation of hematopoietic cells; Primary bone marrow defect

Essential Thrombocytosis

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Do not manifest bleeding tendencies; result of underlying conditions

Secondary Thrombocytosis

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Chronic blood loss due to ineffective regulation of thrombopoiesis by iron

Iron-deficiency Anemia

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Autoimmune disorder (rheumatoid
fever/arthritis)

Chronic Inflammatory Disease

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Bruising; large, irregularly-shaped hemorrhage

Ecchymosis

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Known as stress platelets, appear in compensation for thrombocytopenia

Reticulated platelets

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Increase risk of significant bleeding

< 50,000 μL

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Risk of severe spontaneous bleeding

< 10,000 μL

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Decreased in number of megakaryocytes; due to bone marrow aplasia/hypoplasia

Thrombocytopenia: Decreased Production

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Bone marrow is infiltrated by fibrotic tissue (tumor) which infect the cells

Myelophthisis

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Kills cancer cell but also damages normal cells

Radiation / chemotherapy

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50% of patient only has 6 months to live; difficult for recovery due to bone marrow damage

Aplastic anemia

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Thiazide
Chlorothiazide
Chloramphenicol

Bone Marrow Suppressants

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Production is good; circulation is defective

Thrombocytopenia: Ineffective Production

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Abnormal platelet structure; increased destruction

Hereditary Thrombocytopenia

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FAB M6

Di Guglielmo’s Syndrome (erythroleukemia)

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Involved in development of all nuclear cell maturation

Vitamin B12 or Folate

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Dohle-like inclusions in neutrophil; large/giant platelets

May-Hegglin Anomaly

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Overproduction of platelet being stored in spleen; not enough in circulation

Hypersplenism/Splenomegaly

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Vascular shunting

Hypothermia

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Platelets (primary hemostasis) and coagulation factor (secondary hemostasis); no bone marrow defect but in circulation

Thrombocytopenia: Consumption - Combined

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Excessive clot formation and clot
lysis repetitively

Disseminated Intravascular Coagulation

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Appearance of ultra large vWF (activates platelets which then causes platelet plug formation)

Thrombotic thrombocytopenic purpura (TTP); Moschkowitz Syndrome

Infection of Shiga-like toxin (1 and 2), E. coli O157:H7, Shiga toxin (produced by Shigella spp.) – which causes abnormal consumption due to G.I. bleeding

Hemolytic Uremic Syndrome

Production of antiplatelets Ab (alloantibodies and autoantibodies)

Thrombocytopenia: Immune Destruction

Platelet autoantibodies

Idiopathic thrombocytopenic purpura (ITP)

ITP: Children; during infection & post-vaccination

Acute ITP

ITP: Adult; during platelet autoantibodies

Chronic ITP

Multiple transfusion; develops antibodies from foreign body fluid (blood) like donor to recipient

Post-transfusion purpura

Maternal Ab; neotanal immune-mediated thrombocytopenia; mother produces antibody against infections while having a fetus - mother develop IgG against fetus which has inherited father antigen

Isoimmune neonatal purpura

Develop antibody from self

Autoimmune

Develop antibody from different species

Alloimmune

Mimics ITP

HIV infection

Physical manifestation; enlarged spleen; larger number of platelet sequestrated

Gaucher’s Disease

Rare bone marrow cancer

Myelofibrosis/Osteomyelofibrosis

Seen after multiple blood transfusion (prolonged platelet storage that are dysfunctional/function-depleted)

Dilutional Thrombocytopenia

Adhesion disorder; autosomal recessive disorder affecting the membrane receptor, GpIb

Bernard-Soulier Syndrome

Aggregation disorder; autosomal recessive disorder affecting the receptor complex GpIIb-IIIa preventing the binding of fibrinogen

Glanzmann’s Thrombastenia

Caused by mutation in the gene that controls production of melanosomes, platelet dense bodies, and lysosomes

Hermansky-Pudlak Syndrome

Characterized by giant cytoplasmic granules and decreased ADP released; manifestations include ocular, neurologic, and skin abnormalities, possible neutropenia, normal platelet count but diminished aggregation response

Chediak-Higashi Syndrome

X-linked disorder highlighted by thrombocytopenia, recurrent infections, eczema, and a predisposition to secondary leukemia or lymphoma

Wiskott-Aldrich Syndrome

Characterized by the finding of large platelets that lack α-granules producing a gray appearance on a Wright-stained smear

Gray Platelet Syndrome

Characterized by abnormal proteolysis of α-granules and selective defective aggregation with epinephrine

Quebec Platelet Disorder

Defect in thromboxane generation by abnormal response to arachidonic acid; platelet count may be normal

Cyclooxygenase Deficiency

Defect in platelet coagulant activity caused by impaired transmembrane migration of the procoagulant; PS resulting in the absence of Xa-binding sites

Membrane Phospholipid Deficiency

Platelets will not adhere due to lacking VWF

Von Willebrand’s Disease

No fibrinogen

Afibrinogenemia

Defective or abnormal fibrinogen

Dysfibrinogenemia

Also known as “acetylsalicylic acid”; inhibits cyclooxygenase

Aspirin Intake

Platelet dysfunction results from coating of the platelet membrane by paraprotein and does not depend on the type of paraprotein present

Multiple Myeloma and Waldenstrom’s Macroglobulinemia

Induces thrombocytopenia and a severe platelet function defect that assumes major importance in relation to post-surgical bleeding – platelet count is low

Cardiopulmonary Bypass Surgery

Reduced platelet adhesion, abnormal platelet aggregation (in response to ADP, epinephrine, and thrombin), abnormal phospholipid availability, and reduced procoagulant activity

Liver Disease

“Devil’s pinches”; Skin fragility; Every time you bump on the chair – vessels injured

Simple Purpura

Release tissue thromboplastin

Extrinsic problem

Excessive collagen

Keloid

Sudden increase on body’s pressure – extravasation of RBCs

Mechanical Purpura

Emotional trauma (accident, loss, injury); Hormonal changes in the body; creating permeability to blood vessels

Psychogenic Purpura

Brown spots; As we grow old, formation of collagen slows down – normal process in the body

Senile Purpura

Progressive pigmented purpura; cayenne pepper purpura appearance

Schamberg’s Purpura

Self-induced trauma

Factitious Purpura

Caused by bacterial, fungal, viral and parasitic microorganisms; releases toxins which damages blood vessels

Infectious Purpura

Unique infectious purpura disorder affecting the vessel

Purpura fulminans

Caused by Neisseria meningitis; Excessive lysis and formation

Waterhouse-Friedrichsen Syndrome

Allergic vasculitis (IgA) involves the skin affecting, GIT, kidneys, heart, joint problems and CNS (autoimmune process); common in children, might exist as single disease or may coexist

Henoch-Schonlein Purpura

Abdominal pain, secondary to GIT bleeding

Henoch Purpura

Secondary to joint pain, rheumatoid arthritis, loss of cartilage in joints

Schonlein Purpura

Causes gum bleeding or gingivitis

Scurvy (Vitamin C Deficiency)

Lack of insulin/inhibitors of insulin; increase concentration of sugar in blood; slows down blood flow and destroy blood vessels

Diabetes Mellitus

Causes abnormal enlargement of muscle/vessel, increased testosterone; described by difference in face, shoulders and pink or purple stretch marks

Cushing Syndrome

Proteins are large and big substances and destroy blood vessels, second to dysproteinemia

Protein C Deficiency

Inability to convert procollagen to collagen; hyperextensible skin, hypermobile joints, joint laxity, fragile tissues, and a bleeding tendency, primarily subcutaneous hematoma formation

Ehler’s Danlos Syndrome

Elastic fibers and blood vessels are not elastic enough; elastic fiber calcification, prone to fragility

Pseudoxanthoma Elasticum

Elongated extremities and fingers, not proportional to patient bodies; mutation in the FBN1 gene that codes fibrillin

Marfan Syndrome

Soft and fragile, incomplete formation of bone; mutation in type I collagen genes

Osteogenesis Imperfecta

The vascular defect of this disorder is characterized by thin-walled blood vessels with a discontinuous endothelium; most common blood vessel disorder; lesions on skin, lips and tongue; thin-dilated vessels; caused by Iron Deficiency Anemia

Hereditary Hemorrhagic-Telangiectasia

Another term for Hereditary Hemorrhagic-Telangiectasia

Rendu-Osler-Weber Sydrome

Vascular tumor which blocks functions of blood vessels and destroy them; “Kasabach-Merritt Syndrome”; associated with acute or chronic DIC and MAHA

Congenital Hemangiomata

The deposition of abnormal quantities of amyloid protein in tissues; heavy metal poisoning

Amyloidosis

Excessive destruction of own cells by your own antibody; can be caused by either allergic reaction or drug-induced endothelial damage; drug-induced purpura

Autoimmune Vascular Purpura

Lecture: Platelet and Hemostatic Disorder Flashcards

(81 cards)