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29 Cards in this Set

  • Front
  • Back

Leukopenia

Condition without white blood cells

Types of granulocytes

Neutrophils


Eosinophils


Basophils


Subclasses of lymphocytes

Natural killer


B-lymphocytes


T-lymphocytes

Classes of T-lymphocytes

Regulatory


Cytotoxic


Helper


Neutrophils function

First line of defense against bacteria, kill with superoxide and phagocytize bacteria involved in infections


against bacteria, kill with superoxide and phagocytize bacteria involved in infections


and phagocytize bacteria involved in infections


Eosinophils function

Eosinophils attack parasites, attach to their surface and release substances to kill them, usually superoxide and hydrolytic enzymes



Inactivate substances released by Basophils and mast cells during allergic reactions

Basophils function

Similar to large mast cells that are numerous in the skin, GI tract, and respiratory tract.


Release histamine and heparin when activated my T-lymphocytes.


Important in inflammation

Monocyte function

Very large leukocytes


Become tissue macrophages, together with neutrophils they are the phagocytes of the body, mostly in skin, spleen, liver, lungs, and bone where they become osteoclasts-differentiate into dendritic cells

Hematopoiesis

Blood cell formation

Lymphoid stem cells give rise to...

Lymphocytes

Myeloid stem cells give rise to....

Continually grow into erythrocytes, megakaryocytes, granulocytes or monocytes

Hemorrhagic anemia

Loss of blood

Aplastic anemia

Bone marrow loses capacity to produce RBC (chernobyl was a big cause)

Iron deficiency anemia

RBC are small with low hemoglobin

Pernicious anemia

Lack of vitamin B-12

Sickle cell anemia

Abnormal RBC shape

Hemolytic anemia

Result of hemolytic disease of newborn

Leukemia

Malignant disease of the hematopoeitic tissue in the bone marrow-many types-all caused by a cancerous mutation of the cells in the bone marrow-generally affect WBC

Acute leukemia cause and symptoms

Rapid increase in the number of immature blood cells-over population of immature blood cells makes the bone marrow unable to produce healthy blood cells



Weakness, abnormal bleeding, shortness of breath, flu like symptoms, weight loss, appetite lots, swollen or bleeding gums, anemia, bruising,

Chronic leukemia cause

Slow, excessive build up of relatively mature but abnormal blood cells. Resulting in abnormal white blood cells in the blood

Transport of gasses in blood

-97% oxygen carried bound to hemoglobin in the erythrocytes


-when oxygen binds to hemoglobin it turns red and is called oxyhemoglobin


-Carbon dioxide is carried dissolved in plasma


-CO2 also carried bound to hemoglobin called carbaminohemoglobin

CO2 Transport

Step 1: when CO2 dissolves in plasma, some is made into carbonic acid. Reaction takes place fast because of carbonic anhydrase


Step 2:H2CO3 dissociates into H+ and HCO3-


Step 3: Hydrogen ions are removed by combining with enormous amount of hemoglobin in the RBC


Step 4: HCO3- diffuse out of RBC into plasma


Step5: chloride ions diffuse into RBC from plasma-effect called the chloride shift

Thrombopoietin

Stimulates production of megakaryocytes

Contents of platelets

Actin and myosin


Glycogen


Organelles such as mitochondria and lysosomes


Granules in platelet cytoplasm contain serotonin, von Willebrand factor, clotting factor, and plate derived growth factor

Hemostasis

Prevention of blood loss

Steps in hemostasis

1: temporary local vasoconstriction of damaged arterioles or small arteries


2: accumulation and activation of platelets at the site of damage-formation of platelet plug


3: activation of blood clotting (coagulation)


4: blood clot invaded by fibroblasts and replaced by fibrous tissue, closing the hole permanently and forming scar tissue


Formation of a platelet plug

-Platelets adhere to injured area(von Willebrand factor helps adhere them)


-platelets activate and aggregate together (being exposed to thrombin activates platelet to form a plug


-platelets degranulate and release the contents of granules (change shape and release contents)


Intrinsic pathway

Foreign, negatively charged surfaces (collagen) activate a series of contact activation factors that include IX. Factor IX forms a complex with factor VIII on the platelet surfaces



Stuart factor X and V on platelet surface



Prothrombin + calcium=thrombin



Thrombin activates factor XIII which stabilizes and cross links fibrin



Fibrinogen+thrombin=fibrin

Extrinsic pathway (vascular injury)


Physiologically more important

Tissue factor on fibroblasts and smooth muscle cells binds to and activates factor VIII



Stuart factor X and V on platelet surfaceProthrombin + calcium=thrombinThrombin activates factor XIII which stabilizes and cross links fibrinFibrinogen+thrombin=fibrin