17 10-19 Flashcards
Classes of Leukocytes
Granulocytes, Agranulocytes
Structural characteristics of leukocytes
3
Only formed elements that are complete cells - have nucleus and other organelles.
1.5-3x bigger than RBCs,
less than 1% of blood volume.
Function of leukocytes
Protect from bacteria, viruses, parasites, toxins, tumor cells
4 characteristics of circulating WBCs
- Can migrate out of the bloodstream (diapedesis), but most are found in tissues
- All are capable of amoeboid movement
- All are attracted to specific chemical stimuli (positive chemotaxis)
- Neutrophils/monocytes/macrophages are capable of phagocytosis
Leukocytosis
A WBC count of over 11k - normal in a homeostatic response to an infection.
Leukocytes in order from most to least abundant
Never let monkeys eat bananas
Granulocytes
4
Neutrophils/eosinophils/basophils.
Lobed nuclei (round with connecting strand),
granules stain visibly,
all phagocytic to some degree
Agranulocytes
Lymphocytes/monocytes. Lack visible granulocytes
Neutrophils
4
Actively phagocytize bacteria
chemically attracted to sites of inflammation,
multilobed nucleus (PMN),
granules contain defensin, respiratory burst.
Eosinophils
4
Kill parasitic worms with enzymes
phagocytize antigen-antibody complexes
are involved in allergic reaction by promoting inflammation,
levels often high in autoimmune/eczema
Basophils
5
Release histamine and other mediators.
Found in CT,
promote vasodilation in inflammation
Release heparin (anticoagulant) to inhibit blood clotting,
similar to mast cells (both bind to IgE) but arise from different cell,
Lymphocytes
4
Mount immune response by direct cell attack or via antibodies.
nucleus most of cell volume,
Includes T-lymphocytes/B-lymphocytes/NK cells,
hang out in lymphatic tissue
T cells
Manage and direct immune response and specialize in cellular immunity.
Act directly against virus-infected and tumor cells.
B cells
Play a role in humoral immunity.
Give rise to plasma cells which produce antibodies/immunoglobulins.
NK cells
Defense against infected and abnormal body cells.
Monocytes
Phagocytosis, develop into macrophages.
3-8% of leukocytes,
largest leukocytes,
kidney shaped nucleus,
“big eater” of bacteria/viruses/dead cells,
activate T cells.
New monocytes circulate in the blood for only a few hours before they migrate into the tissue to become macrophages. Some macrophages are fixed - some wander.
Leukopoiesis
4 different CSFs (colony stimulating factors) have been identified that stimulate formation of WBCs.
Interleukins are involved in leukopoiesis.
Differentiation occurs along two pathways: Lymphoid and Myeloid stem cells.
Hematopoietic stem cell/hemocytoblast –> myeloid or lymphoid
Leukopenia
Abnormally low WBC count
Leukemia
Clones of a single WBC that remain unspecialized and divide out of control.
Infectious mononucleosis
WBC issue arising from Epstein-Barr. Viral
Structure of platelets. 4
Not cells in a strict sense - they are cytoplasmic fragments of megakaryocytes.
Smaller than RBCs
contain mitochondria/SER but no nucleus (and age quickly because no nucleus).
Granules contain chemicals that aid in clotting process.
Function of platelets
Critical to clotting process - form seal/plug when a blood vessel breaks. Seal small tears in blood vessels.
Thrombopoiesis
2 points, 3 steps
Hormone thrompoietin regulates formation.
Repeated mitoses of the megakaryocytes without cytokinesis.
- Megakaryocyte presses against a sinusoidand sends cytoplasmic extensions thru.
- Extensions rupture releasing fragments into the blood.
- Plasma membranes seal around the cytoplasm to form platelets.
Hemostasis
Fast, localized response to reduce blood loss through clotting. Squeeze/plug/clot
Hemostasis steps. 3
- Vascular spasms
- Platelet plug formation/platelet phase
- Coagulation
Vascular spasms
Immediate vasoconstriction response to blood vessel injury. Lasts 30 min
Platelet plug formation. 5
Adhesion - When endothelium is damaged, the underlying collagen fibers are exposed and platelets adhere.
Platelets have granules that contain ADP/serotonin/epi/theomboxane. - this soup increases aggregation and vascular spasm.
Aggregation -A positive fb loop happens - more platelets stick and release chems
vWf (von Willebrand factor) is a plasma protein that stabilizes the clinging platelets by bridging them with the collagen.
Normal/undamaged endothelium is lined with prostacyclin/NO which prevents platelet aggregation where the plug isn’t needed.
Coagulation
Or Blood clotting…
a multistep process in which blood is transformed from liquid to gel. Reinforces the platelet plug with fibrin.
3 phases of coagulation
- Formation of prothrombin activator. Extrinsic/intrinsic
- conversion of prothrombin to thrombin
- formation of fibrin mesh from fibrinogen in the plasma
Difference between intrinsic and extrinsic coagulation
Intrinsic: Damage to the inside of a vessel. All factors necessary are present within the blood. Slower clotting pathway, may be triggered by neg charged surfaces.
Extrinsic: Damage to tissue outside the vessel. Triggered by endothelium-derived protein factor TF (tissue factor/factor III) and can happen very rapidly - 15s!
vWf
von Willebrand factor.
Secreted by megakaryocytes/platelets/endothelial cells.
Bridges platelets to collagen in platelet plug formation.
Clotting factors
or procoagulants…
Promote clotting (Numbered I-XIII)
Also calcium, vit K, platelets
Clot retraction - what is it, how does it work?
Process in which the contractile proteins within platelets contract and pull on neighboring fibrin strands, squeezing plasma from the clot and pulling damaged tissue edges together.
As this is happening, PDGF released by platelets stimulates smooth muscle and fibroblasts to rebuild vessel walls.
Fibrinolysis - what happens?, when does it happen?
Removes clots through the action of the fibrin-digesting enzyme plasmin.
When plasminogen is activated (by thrombin and tissue plaminogen activator (t-PA)it produces plasmin.
Factors that limit clot production and prevent undesirable clotting.
3
Heparin, aspirin, prostacyclin
Heparin - released by? What is it?
Released by basophils and mast cells.
Cofactor that accelerates the activation of antithrombin III that inhibits several clotting facts inc. thrombin.
Aspirin does?
Inhibits the production of thromboxane A2 and prostaglandins preventing platelet aggregation
Prostacyclin - when is it released, what does it do?
Released during platelet phase - inhibits aggregation and opposes action of thrombin/ADP/other factors.
Hemostatic disorders?
4
Thromboembolytic disorders
Disseminated intravascular coagulation,
Bleeding disorders,
hemophilia
Thromboembolytic disorders result from?
Thromboembolytic disorders result from conditions that cause undesirable clotting (roughening of vessel/slow flowing blood).
Disseminated intravascular coagulation leads to?
Disseminated intravascular coagulation leads to widespread clotting - complication of pregnancy, incompatible blood transusions.
Bleeding disorders arise from?
Arise from abnormalities that prevent normal clot formation: deficient platelets, lack of synthesis of procoagulants, ↓ vit K, hemophilia
Hemophilia is?
Group of bleeding disorders caused by genetic mutations. Hemophilia A: deficiency or missing factor VIII Hemophilia B: Deficiancy in factor IX.
Agglutinogen is also known as?
Surface antigen
Blood types are based on? What else is present in the blood in relation to these?
Are based on specific antigens on RBC membranes.
Preformed antibodies/agglutinins are present in blood plasma and do not match the individual’s blood.
ABO types are based on?
ABO types are based on the presence/absence of 2 types of agglutinogens (surface antigens) - A and B.
O type
has neither agglutinogen (universal donor)
AB type
Has both agglutinogens (universal recipient)
A type
Has A agglutinogen/surface antigen
B type
Has B agglutinogen/surface antigen
Agglutinins are? They act against?
Preformed antibodies in the plasma. Act against RBCs that are carrying ABO antigens/agglutinogens that are not present on a person’s own RBCs.
Rh factor is?
Surface antigen D - a group of RBC antigens that are either present (Rh+) or absent (Rh-).
What happens if mismatched blood is transfused?
The infused blood is attacked by the recipient’s blood plasma aggluinins resulting in agglutination and hemolysis of the donor cells.
HDN
Hemolytic disease of newborn. Rh- mother, Rh+ - mother’s antibodies will pass thru placenta and destroy baby’s RBCs
Thrombin
Enzyme that induces clotting by converting fibrinogen into fibrin
Thrombus
A clot that develops and persists in an unbroken vessel.
Embolism
Obstruction of a blood vessel by an embolus (blood clot, fatty mass, bubble of air, other debris) floating in the blood.
plasmin
fibrin-digesting enzyme .
Prostacyclin
Normal/undamaged endothelium is lined with prostacyclin which prevents pletelet aggregation.
