Patho Hematology 2

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Have multiple nuclei

Granular

known as “phils”, “poly”, or “seg”

Granular

Agranular “cytes”

Lymphocytes and Monocytes

Neutrophils, Eosinophils, Basophils

Granular

Stored 6 day supply

Lifespan of WBC

Circulate for weeks to months

Lymphocytes

Circulate 10-20 hours then deposit in tissues

Monocytes

Can survive for months

Macrophages

Survive in blood 4-8 hours; survive in tissue 4-5 days

Granulocytes

Identify and neutralize antigen, develop T & B cells, seen in infections and inflammation, low levels in chemotherapy, lymphoma, and steroids

Lymphocytes

Main role - phagocytosis; seen in myelodysplasia, Protozoa, and Rickettsial Disease.

Monocytes

First Responders in early inflammation, common in bacterial infections

Neutrophils

Engulf parasites, regulate mast cells, and common in allergic reactions

Eosinophils

Overproduction of leukocytes leads to overcrowded bone marrow leads to decreased hematopoietic cell production.

Leukemia

Increased leukocyte level with decreased in all other cell lines

Leukemia

Overflow of bone marrow in Leukemia can damage:

Liver, Spleen, Lymph Nodes, CNS

Blast Cells Present

Acute Leukemia

Well differentiated cells

Chronic Leukemia

Too many lymphoblasts

Lymphocytic Leukemia

Too many Myeloblasts

Myelogenous Leukemia

Typical in adults and asymptomatic at diagnosis

Chronic Leukemias

ALL and CML associated with:

Philadelphia Chromosome

AML associated with:

Epigenetics

More susceptible to encapsulated infections r/t B-cell maturation failure

CLL

Malignant proliferation of lymphocytes in the lymphatic system

Lymphomas

Present with swollen lymph nodes, fatigue, weight loss, abdominal swelling, puritis.

Lymphomas

Classic sign for Hodgkin Lymphoma

Reed-Sternberg Cells

Involves only B Cells with a poor prognosis

Hodgkin Lymphoma

Involvemment in B-, T-, and NK cells, and associated with (EBV, HHV-8, HIV, Hep C) and immunosuppression

Non-Hodgkin Lymphoma

Pediatric disease with B-cell neoplasm, EBV, tumors of jaw, facial bones, or abdomen

Burkitts Lymphoma

Slow proliferation in bone marrow. Increased IgG with Bence Jones Protein in urine

Multiple Myeloma

Bone Lesions from malignant cells stimulates hepatic growth factor and parathyroid hormone to increase cytokine production to activate osteoclasts causes increased bone reabsorption

Multiple Myeloma

Risk for bone fractures and renal failure r/t increased serum calcium

Multiple Myeloma

Prevention of blood loss vascular spasm, and formation of platelet plug and fibrous clot.

Homeostatis

Local vasoconstriction causes humoral response to activate substances from vessel endothelium. Platlets arrive and secrete TXA2.

Homeostatis Vascular Constriction (1st step)

Thromboxane A2 (TXA2)

Stimulates platelet expression and aggregation. Aspirin inhibits TXA2.

Adhesion then Activation then Aggregation

Platlet Plug Formation (2nd response in Homeostatis)

Platlets adhere to exposed collagen then become sticky and adhere more tightly to collagen and von Willebrand Factor.

Adhesion

Platelets change shape (pseudopods) and activate arachidonic pathway.

Activation

Induced by TXA2 and coagulation factors to stabilize the platelet plug

Aggregation

Coagulation cascade triggered in 15-20 seconds

Trauma

Coagulation cascade triggered in 1-2 minutes

Ineffective platelet plug

Platelet aggregation and fibrin thread form a true clot

3-6 minutes

Clot retracts to further occlude

20-60 minutes

Primary Clotting Pathway, measured by PT

Extrinsic Pathway

Supports and amplifies extrinsic pathway, measured by PTT

Intrinsic Pathway

Important in clotting cascade involving platelet activation and converting intrinsic factors to active forms

Calcium

Vascular damage prothrombin activator forms that triggers coversion of prothrombin to thrombin that converts fibrinogen to fibrin to form clot.

Common pathway for extrinsic and intrinsic

Regulated by thrombin and plasminogen

Clot dissolution

Antithrombin III (AT3) blocks thrombin from activating fibrinogen. Heparin works with AT3 to remove thrombin, XIIa, XIa, Xa.

Removal of Thrombin from blood

Tissue plasminogen activator (t-PA) released and converts plasminogen to plasmin

Clot removal after vessel has healed

Digests fibrin, fibrinogen, prothrombin, Factors V, VIII, XII

Proteolytic enzyme

Levels of fibrinogen, Factors V, VII, IX, vWF, and platelet activation all increase

Aging

von Willebrand Disease

Inherited clotting disease

Factor V Liden, Protein C deficiency, Protein S deficiency

Inherited Hypercoagulable Disease

Uremia

Acquired clotting disease

Antiphospholipid Ab, Cancer, Pregnancy

Acquired Hypercoagulable Disease

Venous Stasis, Vessel Damage, Hypercoagulable State

Virchow Triad

Risk for clot dislodgement and embolus

Proximal to DVT

Autosomal dominant, resistance to protein C causing excess thrombin

Factor V Liden

Autoimmune Abs attack plasma proteins and clothing factors, more common in women

Antiphospholipid Syndrome

Inherited (genetic or autoimmune) with high amounts of vWF. platelets stick to each other causing anemia, thrombocytopenia, and microvascular thrombi

Thrombotic Thrombocytopenia Purpura (TTP)

Acquired (Viral, time-limited) peripheral problem (bone marrow still makes platelets). PLT phagocytosis by macrophages to CD4 to IgG. associated with HIT

Primary Immune (Idiopathic) Thrombocytopenia Purpura (ITP)

Rare, autoantibodies to factor VIII

Acquired Hemophilia

Hemophilia A and B

Inherited

Prolonged aPTT but normal PLT and PT

Hemophilia A and B

Hemophilia A and B associated with what clotting pathway?

Intrinsic

Deficiency in factor IX

Hemophilia B

Deficiency in factor VIII, most common hemophilia

Hemophilia A

Most common inherited bleeding disorder, decreased vWF which decreases PLT adhesion and increased bleeding

von Willebrand Disease

Contrast von Willebrand Disease with TTP

von Willebrand Disease has decreased vWF while TTP had elevated vWF

Stage of DIC: Increased procoagulants (tissue factor) with widespread endothelial injury causing microvascular clots

Procoagulable

Overconsumption of clotting factors and PLT

Source of DIC Bleeding

Plasmin activation (degrades fibrin and clotting factors) to degrade clot

Source of Bleeding in DIC

Decreased PLT and clotting factors. Increased PT, PTT, and D-Dimer.

Labs with DIC

PT, PTT, and D-dimer are increased in DIC because?

Not enough clotting factors and it’s taking longer for clotting response to work

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