Chapter 17- Blood Flashcards
Functions of blood
- Distribution of:
- > oxygen and nutrients to body cells
- >metabolic wastes to the lungs and kidneys for elimination
- > hormones from endocrine organs to target organs - Regulation of:
- >Body temperature (by absorbing and distributing heat
- >maintain normal pH (7.35-7.45) using buffers
- >adequate fluid volume in the circulatory system - Protection against
- >blood loss– plasma proteins and platelets initiate clot formation
- > infection– antibodies, complement proteins, WBCs defend against foreign invaders
Functions of blood- distribution
- Distribution of:
- > oxygen and nutrients to body cells
- >metabolic wastes to the lungs and kidneys for elimination
- > hormones from endocrine organs to target organs
Functions of blood- regulation
- Regulation of:
- >Body temperature (by absorbing and distributing heat
- >maintain normal pH (7.35-7.45) using buffers
- >adequate fluid volume in the circulatory system
Functions of blood- protection
- Protection against
- >blood loss– plasma proteins and platelets initiate clot formation
- > infection– antibodies, complement proteins, WBCs defend against foreign invaders
Blood composition
- > Fluid connective tissue composed of
- plasma (55% of blood)
*formed elements (45% blood of blood)
*erythrocytes (red blood cells):
-Hematocrit:
percent of blood volume that is in RBCs. 47% plus/minus 5% for males. 42% plus/minus 5% for females
- leukocytes (white blood cells)
- platelets
- > pH 7.35-7.45 (slightly basic)
hematocrit (Hct)
RBC/total blood volume
Formed elements when blood drawn and put into a centrifuge
Plasma:
- 55% of whole blood
- least dense component
Biffy coat:
- leukocytes and platelets
- <1% of whole blood
Erythrocytes:
- 45% of whole blood
- most dense component
Hematopoiesis
Hemopoiesis:
- blood cell formation
- occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur
Hemocytoblasts (hematopoietic stem cells):
- give rise to all formed elements
- hormones and growth factors push the cell toward specific pathway of blood cell development
Hemocytoblasts
- > hematopoietic stem cells
- > give rise to all formed elements
- > hormones and growth factors push the cell toward a specific pathway of blood cell development
Erythropoiesis
-red blood cell production
hemocytoblast-> erythrocyte
takes 15 days. color changes from blue of ribosomes to pink of hemoglobin
Regulation of erythropoiesis
- > too few RBCs leads to tissue hypoxia
- > too many RBCs increases blood viscosity
balance between RBC production and destruction depends on:
- hormonal controls
- adequate supplies of iron, amino acids, and B vitamins
Hormonal control of erythropoiesis
Erythropoietin (EPO):
- hormone that stimulates erythropoiesis
- released by the kidneys in response to hypoxia
Effects of EPO:
- increases production of RBCs
- testosterone also enhances EPO production, resulting in higher RBC counts in males (Lance Armstrong scandal)
Dietary requirements:
- Nutrients
- iron
- Vitamin B12
- Folic acid
Erythropoietin (EPO)
Erythropoietin (EPO):
- hormone that stimulates erythropoiesis (red blood cell production)
- released by the kidneys in response to hypoxia
Effects of erythropoietin (EPO)
Effects of EPO:
- increases production of RBCs
- testosterone also enhances EPO production, resulting in higher RBC counts in males (Lance Armstrong scandal)
Negative feedback cycle
1 Stimulus:
-Hypoxia (low blood oxygen carrying ability) due to– decreased RBC count, decreased amount of hemoglobin, decreased availability of oxygen
2 Kidney (and liver to a smaller extent) releases erythropoietin
- Erythropoietin stimulates red bone marrow
4 enhanced erythropoiesis increases RBC count
5 Oxygen carrying ability of blood increases
Leukopoiesis
- Production of white blood cells
- stimulated by chemical messengers from bone marrow and mature WBCs
- all leukocytes originate from hemocytoblasts
- there are 5 main types of WBCs
(many of the hematopoietic hormones (EPO) are used with cancer or AIDS patients to stimulate bone marrow
Blood plasma (90-92% water)
- > Plasma proteins- contribute to osmotic pressure, most common is albumin
- > Nitrogenous by-products of metabolism- lactic acid, urea, and creatinine
- > Nutrients- glucose, lipids, amino acids, vitamins
- > electrolytes- Na+, K+Ca+, Mg+, Cl-, HCO3-…. most abundant
- > respiratory gases- oxygens and CO2
- > hormones
Formed elements
-> RBC, WBC, and platelets
- > RBC majority of formed elements (99%)
- RBCs have no nuclei or organelles
- > only WBCs are complete cells
- > platelets are cell fragments
- > most blood cells originate in bone marrow and do not divide
Erythrocyte structure and function
- > RBCs are dedicated to respiratory gas transport
- biconcave discs, no nucleus, no organelles
- > hemoglobin binds reversibly with oxygen
- > iron atom in each heme can bind to one oxygen molecule
- > Each hemoglobin can transport 4 oxygens
Life of a RBC
- > Birth: red bone marrow. 15 days to grow
- > lives for about 120 days
- > dies in the SPLEEN, macrophages destroy old and damaged RBCs
- > hemoglobin is broken down and parts are either recycled or excreted
Erythrocyte disorders
- Anemia:
- low oxygen carrying capacity causes: blood loss, low RBCs produced, abnormal RBC - Polycythemia: excess of RBC (increases viscosity)
- > bone marrow cancer
- >secondary polycythemia- when oxygen is available (high altitude) or when EPO production increases
- >blood doping- causes increase risk of MI, stroke or blood clots
Anemia
-low oxygen carrying capacity causes: blood loss, low RBCs produced, abnormal RBC
Polycythemia
excess of RBC (increases viscosity)
- > bone marrow cancer
- > secondary polycythemia- when oxygen is available (high altitude) or when EPO production increases
- > blood doping- causes increase risk of MI, stroke or blood clots
causes of anemia
- Blood loss- hemorrhagic anemia
- Not enough RBC produced:
* Pernicious anemia: vitamin B12, intrinsic factor
* Aplastic anemia: destruction of bone marrow by drugs - RBC destroyed orr abnormal hemoglobin:
* hemolytic anemia- mismatched blood
- thalassemias- genetic disease of mediterranean ancestry
- sickle cell anemia: abnormal hemoglobin
Leukocytes
- > Make up less 1% of total blood volume
- > can leave capillaries via diapedesis
- > move through tissue spaces by ameboid motion and positive chemotaxis (follows trail released by damaged cells)
- > leukocytosis: WBC count over 11,000 (normal response to bacterial or viral invasion)
Granulocytes
- > Granulocytes:
- neutrophils
- eosinophils
- basophils
- > cytoplasmic granules stain specifically with Wright’s stain
- > larger and shorter-lived than RBCs
- > lobed nuclei
- > 1st stand during an infection, they attack in large numbers and eat until they die. “phagocytic”
- > ex: pus in an infected wound are dead granulocytes
Granulocytes
- > Neutrophils:
- bacteria slayers- phagocytic
- most numerous
- > eosinophils:
- digest parasitic worms
- elevated with allergies
- phagocytic
- > Basophils:
- contain histamine
- promotes inflammation
Neutrophils
- > Granulocyte
- bacteria slayers- phagocytic
- most numerous
eosinophils
- > granulocyte
- digest parasitic worms
- elevated with allergies
- phagocytic
Basophils
- > granulocyte
- contain histamine
- promotes inflammation
Agranulocytes (no granules)
- Lymphocytes
* mostly in lymph tissue
* crucial to immunity
* T cells and B cells - Monocytes
* largest WBC
* “big eaters” against viruses and bacteria
* becomes macrophage when it leaves blood stream
Lymphocytes
-> agranulocyte (no granules)
- mostly in lymph tissue
- crucial to immunity
- T cells and B cells
Monocytes
-> agranulocyte (no granules)
- largest WBC
- “big eaters” against viruses and bacteria
- becomes macrophage when it leaves blood stream (in the tissues)
Leukocyte disorders
- > Leukopenia (penia=poverty)
- abnormally low WBC count–drug induced (usually anti-cancer drugs)
- > Leukemias
- cancerous conditions involving overproduction of WBCs
- WBCs are nonfunctional and cannot defend body
- treatments include irradiation, antileukemic drugs (destroys the rapidly dividing cell), and stem cell transplants
Leukopenia
- > leukocyte disorder
* abnormally low WBC count–drug induced (usually anti-cancer drugs)
Leukemias
- > leukocyte disorder
- cancerous conditions involving overproduction of WBCs
- WBCs are nonfunctional and cannot defend body
- treatments include irradiation, antileukemic drugs (destroys the rapidly dividing cell), and stem cell transplants
Platelets
- > Small fragments of megakaryocytes , not really cells
- > formation is regulated by thrombopoietin (hormone)
- > granules contain many chemicals that aide in clotting process
- > forms a temporary plug in a broken blood vessel
A. Hemostasis
- fast series of reactions for stoppage of bleeding
- vascular spasm
- platelet plug formation
- coagulation (blood clotting)
- Vascular spasm
- this is the first step in hemostasis (stoppage of bleeding)
- vasoconstriction of damaged blood vessel, constricted blood vessel reduces blood loss allowing time for the next 2 steps
- triggers:
- direct injury
- chemicals released by endothelial cells and platelets
- pain reflexes
- platelet plug formation
- this is the second step in hemostasis (stoppage of bleeding)
- positive feedback cycle because as more platelets stick together, there is an increase in chemicals released and more platelets arrive
- at site of blood vessel injury, platelets stick to exposed collagen fibers with the help of clotting factors (a plasma protein)
- coagulation
- this is the third step in hemostasis (stoppage of bleeding)
- a set of reactions in which blood is transformed from a liquid to a gel
- reinforces the platelet plug with fibrin threads, “molecular glue”
- has 3 stages that use clotting factors made in the liver. clotting factors are numbered from I to XIII
coagulation steps
- 3 phases of coagulation:
1. prothrombin activator is formed (intrinsic and extrinsic pathways)
2. prothrombin is converted into thrombin
3. thrombin catalyzes the joining of fibrinogen to form a fibrin mesh - starts with clotting factors and ends with fibrin mesh
B. Clot retraction
- actin and myosin in platelets contract within 30-60 min, draws ruptured edges of blood vessel more closely together
- platelets pull on the fibrin strands, squeezing serum from the clot
C. clot repair
- platelet derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
- growth factors stimulate endothelial cells to multiply and restore the endothelial lining
- new cells grow to repair wound site
D. fibrinolysis
- begins within 2 days, removes unneeded clots
- plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin
- plasmin is a fibrin-digesting enzyme
Clotting overview
A. Hemostasis: stops bleeding
B. clot retraction: draws edges of blood vessel together
C. clot repair: rebuild vessel wall
D. fibrinolysis: plasmin digests fibrin
factors limiting clot growth or formation
- > homeostatic mechanisms prevent clots from becoming large
- swift removal and dilution of clotting factors (swift blood flow)
*inhibition of activated clotting factors
^ most thrombin is bound to fibrin threads, and prevented from acting elsewhere- fibrin acts as an anticoagulant (keeps thrombin local)
^heparin, another anticoagulant, also inhibits thrombin activity
***need to inhibit or inactivate thrombin
factors preventing undesirable clotting
- > platelet adhesion is prevented by:
- smooth endothelial lining of blood vessels
- antithrombic substances: nitric oxide and prostacyclin secreted by endothelial cells
- vitamin E, which acts as a potent anticoagulant
disorders of hemostasis: Thromboembolic
- > Thromboembolic disorders: undesirable clot formation
- Thrombus: stationary clot; DVT
- embolus: travelling clot; PE (becomes an embolism if it wedges in a vessel)
Prevented by blood thinners (ant-coagulants)
disorders of hemostasis: bleeding disorders
- abnormalities that prevent normal clot formation
- thrombocytopenia: decreased # of platelets
- hemophilia: hereditary bleeding disorders
Rh factor
type of protein on surface of RBC
-> 85% of people of Rh+
ABO blood groups
- > Types A, B, AB, and O
- > Based on the presence or absence of two agglutinogens (A and B) on the surface of the RBCs
- > Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present
- > Anti-A or anti-B form in the blood at about 2months of age
hemolytic disease of the newborn
- > Also called erythroblastosis fetalis. Mother is Rh neg and father is Rh +, baby will be Rh+
- > Rh– mother becomes sensitized when exposure to Rh+ blood during delivery & produces anti-Rh antibodies
- > During 2nd pregnancy, antibodies cross the placenta and destroy the RBCs of an Rh+ baby
tranfusion reactions
- occur if mismatched blood is infused
Donor’s cells:
-Are attacked by the recipient’s plasma agglutinins (antibodies)
- Agglutinate and clog small vessels
- Rupture and release free hemoglobin into the bloodstream
- Symptoms: skin flushing, fever, pain
- > Result in:
- Diminished oxygen-carrying capacity
-Hemoglobin in kidney tubules and renal failure
Restoring blood volume
-> Death from shock may result from low blood volume
- > Volume must be replaced immediately with:
- Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition
- Plasma expanders
- -Mimic osmotic properties of albumin (pulls water in)
- -More expensive and may cause significant complications
Hematocrit
oxygenation status
blood glucose tests
metabolic function, increased levels in diabetes
differential WBC count
increased with infections
prothrombin time and platelet counts assess hemostasis- clotting mechanisms
yes
SMAC
a blood chemistry profile (sequential multiple analysis with computer)
complete blood count (CBC)
counts of different formed elements, hematocrit, hemoglobin content and size of RBC
