chp 17. Flashcards
Functions of Blood
- transportation-
- -oxygen from the lungs and nutrients from the intestine to all cells of the body
- -Transport metabolic waste
- -Transport hormones
- regulation
- -Distribute heat around body
- -maintain pH, serve as a bicarbonate reserve
- -maintain fluid volume
- protection
- -excess blood loss (creates blood clots)
- prevent infection(white blood cells)
Spun tube of blood yields three layers:
Erythrocytes on bottom 45% of whole blood
WBCs and platelets in Buffy coat- less than 1%
Plasma on top-55%
Hematocrit
percent of blood volume that is RBCs
formed elements
Buffy coat, erythrocytes
bright red
dark red
oxygenated
deoxygenated
which gender has more blood
adult male 5-6L
adult female 4-5L
pH of blood
and temp
pH= 7.35-7.45= slightly alkaline
temp=100.4
Blood Plasma color and texture
- mostly made up of
- which are most abundant
Straw colored, sticky Water (90% of volume) 100+ Dissolved solutes (hormones, ions, gases, etc.) Proteins are the most abundant solutes Albumin (60% of plasma protein) Blood buffer Shuttles molecules Maintains osmotic pressure
Formed elements detailed
-Erythrocytes (Red-blood cells) Anucleate (without nucleus) -Leukocytes (White-blood cells) Nucleated -Platelets Cell fragments
Erythrocytes description
-spectrin?
- Bioconcave disk
- –large surface area
-no nuclues
- no organalles
- -no O2 consumption
- lots of hemoglobin
- -caries o2, 97% HB
Spectrin
-a cool protein in the plasma membrane that lets the cell change shape
three characteristics of red blood cells that demonstrate form and function relationship
Three features make for efficient gas transport:
- Biconcave shape offers huge surface area relative to volume for gas exchange
- Hemoglobin makes up 97% of cell volume (not counting water)
- RBCs have no mitochondria
- -ATP production is anaerobic, so they do not consume O2 they transport
Hemoglobin consists of
red heme pigment bound to the protein globin
-Globin is composed of four polypeptide chains
Two alpha and two beta chains
-A heme pigment is bonded to each globin chain
Gives blood red color
Each heme’s central iron atom binds one O2
Each Hb molecule can transport
four oxygens
O2 loading in lungs
Produces
oxyhemoglobin (ruby red)
O2 unloading in tissues
Produces
deoxyhemoglobin, or reduced hemoglobin (dark red)
CO2 loading in tissues
20% of CO2 in blood binds to Hb, producing carbaminohemoglobin
word for production of RBC’s and where does it occur
Hematopoiesis (hemopoiesis) occurs in the Red Bone Marrow
All formed elements derived from the ____ cell
hematopoietic stem cell (hemocytoblast)
phases of RBC
hematopoietic stem cell->pro erythroblast->Basophilic erythroblast (phase 1)->polychromatic erythroblast->orthochromatic erythoroblats(phase 2)-> reticulocyte(phase 3)->erythrocyte
too few RBCs lead to
too many RBC lead to
Too few RBCs lead to tissue hypoxia
Too many RBCs increase blood viscosity
Balance between RBC production and destruction depends on:
Hormonal controls
Dietary requirements
Erythropoietin(EPO)
-relased by ____ in response to
hormone that stimulates formation of RBCs
-Always small amount of EPO in blood to maintain basal rate
-Released by kidneys (some from liver) in response to hypoxia
At low O2 levels, oxygen-sensitive enzymes in kidney cells cannot degrade hypoxia-inducible factor (HIF)
HIF can accumulate, which triggers synthesis of EPO
Causes of hypoxia:
- Decreased RBC numbers due to hemorrhage or increased destruction
- Insufficient hemoglobin per RBC (example: iron deficiency)
- Reduced availability of O2 (example: high altitudes or lung problems such as pneumonia)
Too many erythrocytes or high oxygen levels in blood
inhibit EPO production
- EPO causes erythrocytes to mature faster
- -Testosterone enhances EPO production, resulting in higher RBC counts in males
Erythropoietin mechanism
- hypoxia-> kidney releases erythropoietin-> erythropoietin stimulates red bone marrow->enhanced erythropoiesis increases RBC count-> O2-carrying ability of blood rises
Some athletes abuse artificial EPO
Use of EPO
Dangerous consequences:
-increases hematocrit, which allows athlete to increase stamina and performance
- EPO can increase hematocrit from 45% up to even 65%, with dehydration concentrating blood even more
- Blood becomes like sludge and can cause clotting, stroke, or heart failure
Dietary requirements for erythropoiesis
- Amino acids, lipids, and carbohydrates
- Iron: available from diet
- -65% of iron is found in hemoglobin, with the rest in liver, spleen, and bone marrow
- -Free iron ions are toxic so iron is bound with proteins:
- —Stored in cells as ferritin and hemosiderin
- —Transported in blood bound to protein transferrin
- Vitamin B12 and folic acid are necessary for DNA synthesis for rapidly dividing cells such as developing RBCs
RBC’s lifespan
RBC’s engulfed by macrophages
Useful life span of 100-120 days
- often trapped in spleen
- Iron core recycled
- Heme group degraded to bilirubin and taken to liver
- -Secreted in bile and lost
- Globin protein metabolized for its amino acids
Anemia Hemmorgic HEMOLYTIC Aplastic Iron deficiency Pernicious Thalassemias Sickle cell Polycythemia
low oxygen carrying capacity of blood
- Insufficient number of cells
- –Hemmoragic: rapid blood loss
- –Hemolytic: rupture of RBC’s (infection, etc)
- -Aplastic: bone marrow impaired
- Decreased hemoglobin content
- -Iron deficiency (creating microcytes-small pale RBCs)
- -Pernicious: deficiency of B12 (intrinsic factor needed for absorption of vitamin, macrocysts-large pale RBCs)
- Abnormal hemoglobin
- -Thalassemias: faulty globin chains
- -Sickle cell anemia: Change in the beta chain of HbS
- -Polycythemia: excess of RBC’s,
- —-Sometimes due to bone marrow cancer
leukocytes percentage of blood
less than 1% of blood
Leukocytes function
Defense against disease
diapedesis
Leukocytes Able to pass through capillary beds (diapedesis), and move about tissues using amoeboid motion and positive chemotaxis
Classes of Leukocytes
Granulocytes- all phagocytic- Cells have visual granules in cytoplasm -Neutrophils -Basophils -Eosinophils
Agranulocytes -Lack visual granules in cytoplasm -Lymphocytes -Monocytes
Neutrophils
- Very phagocytic
- Most abundant
- 2X size of RBC
- Dye both red and blue
- Granules hold defensins
- -antibiotics
- -Specialize in destroying bacteria
- Nuclei 3-6 lobes (polymorphonuclear)
Eosinophils
-2-4% of all WBC’s
-Bilobed nucleus
-Stain Red
-Granules hold digestive enzymes
—Defense against parasites
(tapeworms,roundworms, etc)
-too large to be phagocytized
-Role in allergies and asthma
Basophils
- 0.5% of all WBC’s; rarest type of WBC
- Bilobed nucleus
- Stains blue with addition of dye
- Release histamine to attract further WBC’s to infected area
Lymphocytes
- Second most numerous WBC
- Large, Spherical nucleus
- Most in tissues, few in bloodstream
- T-lymphocytes: act directly against virus infected cells and tumors
- B-lymphocytes: give rise to plasma cells, which produce antibodies
Monocytes
- 3-8% of WBC’s
- Largest WBC
- U shaped nucleus
- Macrophage function (swallow infected cells) and activate lymphocytes
- Leave circulation and become macrophages
- Very hungry
Leukopoiesis
- production of WBCs are stimulated by two types of chemical messengers from red bone marrow and mature WBCs
- –Interleukins are numbered (e.g., IL-3, IL-5)
- –Colony-stimulating factors (CSFs) are named for WBC type they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
All leukocytes originate from
hemocytoblast stem cell that branches into two pathways:
- Lymphoid stem cells produces lymphocytes
- Myeloid stem cells produce all other elements
Granulocyte production:
stored more in bone or blood?
which are formed more WBC or RBCs?
- Myeloblasts: arise from myeloid line stem cells
- 2.Promyelocytes: accumulate lysosomes - Myelocytes: accumulate granules
- 4.Band cells: nuclei form curved arc - Mature granulocyte: nuclei become segmented before being released in blood
10× more are stored in bone marrow than in blood
3× more WBCs are formed than RBCs, because WBCs have a shorter life, cut short by fighting microbes
Agranulocyte production:
Monocytes: derived from myeloid line
- Monoblast → promonocyte → monocyte
- Share common precursor with neutrophils
- Can live for several months
Lymphocytes: derived from lymphoid line
- T lymphocyte precursors give rise to immature T lymphocytes that mature in thymus
- B lymphocyte precursors give rise to immature B lymphocytes that mature within bone marrow
- Lymphocytes live from a few hours to decades
Platelets are formed from
Platelets function in?
Large cytoplasmic fragments broken off of megakaryocytes
- Megakaryocytes are formed when mega karyoblasts undergo repeated mitosis without cytokinesis
- regulated by thrombopoietin
- Function in blood clotting
Leukocyte disorders
Leukopenia
Leukemia
Infectious mononucleosis
-Leukopenia: low WBC’s (anti-cancer drugs)
- Leukemia: impair normal bone marrow function
- -Over production of abnormal WBC (usually cloning of a single abnormal cell)
- -Acute: fast (from lymphoblasts)
- -Chronic: slow (from myelocytes)
-Infectious mononucleosis: viral disease from the Epstein-barr virus. No cure. Rarely fatal
Formation of Platelets
hematopoietic stem cell-> Megakaryoblast-> Megkrayocyte-> Megakaryocyte(bigger)-> platelets
Control of bleeding
3 steps
Vascular spasm-smooth muscle contracts, causing vasoconstriction
Platelet plug formation-injury to lining f vessel exposes collagen fibers: platelets adhere, platelets release chemicals that make nearby platelets sticky; platelet plug forms
Coagulation-fibrin forms a mesh that traps red blood cells and platelets, from forming the clot
Vascular spams are triggered by
Direct injury to vascular smooth muscle
Chemicals released by endothelial cells and platelets
Pain reflexes
- most effective in smaller blood vessels
- can significantly reduce blood flow until other mechanisms can kick in
-vasoconstriction
prostacyclins and nitric oxide
secreted by endothelial cells act to prevent platelet sticking
-Platelets do not stick to intact vessel walls because collagen is not exposed
_____factor helps to stabilize platelet-collagen adhesion
Von Willebrand
When activated, platelets swell, become spiked and sticky, and release chemical messengers:
-uses what cycle
- ADP causes more platelets to stick and release their contents
- Serotonin and thromboxane A2 enhance vascular spasm and platelet aggregation
-Positive feedback cycle: as more platelets stick, they release more chemicals, which cause more platelets to stick and release more chemicals
Platelet plugs are fine for small vessel tears, but larger breaks in vessels need additional step
Coagulation (blood clotting) reinforces platelet plug with fibrin threads in what kind of vessels?:
Blood is transformed from
Blood clots are effective in sealing larger vessel breaks
-liquuid to gel
Coagulation forms in three phases: phase 1
Phase 1: Two pathways to prothrombin activator
Initiated by either intrinsic or extrinsic pathway (usually both)
-Triggered by tissue-damaging events
-Involves a series of procoagulants
-Each pathway cascades toward and ends with the activation of factorX
FactorX then complexes with Ca2+, PF3 (platelet factor 3), and factorV to form prothrombin activator
Intrinsic pathway (coagulation)
- Called “intrinsic” because clotting factors are present within the blood
- Triggered by negatively charged surfaces such as activated platelets, collagen, or even glass of a test tube
Extrinsic pathway
coagulation
- Called “extrinsic” because factors needed for clotting are located outside blood
- Triggered by exposure to tissue factor (TF); also called factorIII
- Bypasses several steps of intrinsic pathway, so faster pathway
Phase 2: Pathway to thrombin
coagulation
Prothrombin activator catalyzes transformation of prothrombin to active enzyme thrombin
Phase 3: Common pathway to the fibrin mesh
- Thrombin converts soluble fibrinogen to fibrin
- Fibrin strands form structural basis of clot
- Fibrin causes plasma to become a gel-like trap catching formed elements
- Thrombin (along with Ca2+) activates factor XIII (fibrin stabilizing factor), which:
- -Cross-links fibrin
- -Strengthens and stabilizes clot
- Anticoagulants: factors that normally dominate in blood to inhibit coagulation
Thrombocytopenia
deficiency in the number of platelets
Impaired liver function
unable to synthesize procoagulants. Often due to a Vitamin K problem
Hemophilia:
hereditary bleeding disorder
- Factors VIII (type A), IX (type B)
- Sex linked (males get it more often)
- Exercise can cause bleeding in joints
Thrombus
Clot in an unbroken blood vessel
Embolus
Thrombus floating through blood vessel
Embolism
Embolus in a blood vessel too narrow for it to pass through
Transfusions
- A loss of blood greater than 30% (~2-3 liters) can cause severe shock; possibly fatal
- Whole blood transfusions
- Packed red cells (most of plasma removed), with heparin as the anticoagulant
types of blood antigens
Glycoproteins (antigens) located on the surface of RBC’s
There are at least 30 different types of antigens
ex: ABO
ABO blood groups
Based on presence or absence of two agglutinogens (A and B) on surface of RBCs
-Type A has only A agglutinogen
-Type B has only B agglutinogen
-Type AB has both A and B agglutinogens
-Type O has neither A nor B agglutinogens
Blood may contain preformed anti-A or anti-B antibodies
agglutinins)
Act against transfused RBCs with ABO antigens not present on recipient’s RBCs
Rh blood groups
- Rh+ indicates presence of D antigen
- 85% of Americans are Rh+
- Anti-Rh antibodies are not spontaneously formed in Rh negative individuals
- Anti-Rh antibodies form if Rh- individual receives Rh+ blood, or Rh- mom is carrying Rh+ fetus
- Second exposure to Rh+ blood will result in typical transfusion reaction
Antigens promote
gglutination (clumping), and are termed agglutinogens
In the plasma, there are preformed antibodies called agglutinins, which are
unreactive to a persons own red blood cells
universal donor
universal recipients
donor: type o
recipient: type AB
Autologous transfusions:
redonate blood for elective surgery, to avoid transfusion problems and/or disease transmission
Examination of blood can yield information on persons health:
Low hematocrit
Blood glucose
Leukocytosis
Low hematocrit seen in cases of anemia
Blood glucose tests check for diabetes
Leukocytosis can signal infection
Differential WBC count
looks at relative proportions of each WBC
Increases in specific WBC can help with diagnosis
Prothrombin time and platelet counts
assess hemostasis
CMP (comprehensive medical panel):
blood chemistry profile that checks various blood chemical levels
Abnormal results could indicate liver or kidney disorders
Complete blood count (CBC)
checks formed elements, hematocrit, hemoglobin
