chapter 19 - blood
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Chapter 19 - Blood. Functions of Blood. Transportation Delivery of nutrients, hormones Removal of wastes Regulation Body temperature pH Fluid volume Protection Prevent blood loss Prevent infection. Physical Characteristics of Blood. A liquid connective tissue A mixture - PowerPoint PPT PresentationTRANSCRIPT
Chapter 19 - Blood
Functions of Blood Transportation
Delivery of nutrients, hormones Removal of wastes
Regulation Body temperature pH Fluid volume
Protection Prevent blood loss Prevent infection
Physical Characteristics of Blood A liquid connective tissue A mixture
Formed elements - living blood cells Plasma - fluid matrix
Heavier, thicker, more viscous than water Due to ions, plasma proteins, blood cells Composition and volume regulated by hormones
Temp - 38° C, higher than body temperature pH - 7.4 (ranges from 7.35-7.45) Volume differs between sexes, conditional
Female - average 4-5 L Male - average 5-6 L
Components of Blood
Blood sample Spin it Separates into 2 parts
plasma • straw colored liquid on top• 55% of the volume
formed elements • solid portion on bottom
– red blood cells– buffy coat - white blood cells and platelets
45% of the volume Hematocrit
percentage of formed element in a volume of blood about 45% (higher in males than females)
Components of Blood
Blood Plasma Plasma
92% water 7% proteins 1% other solutes
Proteins important (I ) for osmotic balance Albumin Fibrinogen (blood
clotting) Globulins Regulatory
proteins
Blood Plasma
Other solutes Waste products Nutrients Regulatory
substances Gases Electrolytes
Blood Plasma
Formed elements 99% red blood cells 1% white blood cells
and thrombocytes (platelets)
Formed Elements
Erythrocytes - Red Blood Cell's (RBC’s)
IMPORTANT! Note the differences in relative size and appearance!
Formed Elements
Leukocytes - White Blood Cells Granular
leukocytes (granulocytes)
neutrophils eosinophils basophils
Agranular leukocytes (agranulocytes)
lymphocytes - T cells, B cells
Monocytes Thrombocytes -
platelets
Formed Elements
Blood Components
Hematopoiesis - blood cell formation All blood cells come from pluripotent hematopoietic
stem cells (hemocytoblasts) Reside in red bone marrow Give rise to precursor cells which develop into RBC’s,
WBC’s and thrombocytes
Formation of Blood Cells
Formation of Blood Cells
Erythropoiesis RBC production, specifically Hormonally controlled Three phases
production of ribosomes synthesis of hemoglobin ejection of the nucleus and organelles
Leave bone marrow as reticulocyte Mature in blood to a erythrocyte
Regulation of RBC production Regulated by negative feedback
O2 levels monitored in kidneys hypoxia increases RBC production
Production stimulated by erythropoietin (EPO) from kidneys Numbers
M - 5.4 million RBC’s/L (Testosterone stimulates EPO) F - 4.8 million RBC's/L 2 million cells released into blood/second
Anemia - Low O2 carrying capacity of blood Insufficient # of RBC’s
hemorrhage - loss of RBC’s hemolytic anemia - premature RBC rupture due to transfusion,
disease, genetic problems aplastic anemia
• destruction or inhibition of hematopoietic components in bond marrow
• toxins, drugs or irradiation Decreased hemoglobin content
iron (heme) deficiency insufficient iron due to diet or poor absorption
Formation of Blood Cells
Hematocrit % of blood that is RBC’s M 40-54% (47%), F 38-46% (42%), Why? Indicates RBC production and hydration
state Abnormal Hct?
altitude – hypoxia, increased RBC’s athletes - blood doping anemia – decreased RBC’s dehydration
Formation of Blood Cells
Red Blood Cells (Erythrocytes) RBC’s
99% of formed elements
Function to carry O2 Anatomy
Biconcave disks, 8µm in diameter
No nucleus or metabolic machinery
Filled with hemoglobin (Hgb)
O2 carrying protein synthesized in
cytosol before nucleus lost
33% of cell weight
Red Blood Cells (Erythrocytes) Normal Hgb in blood
Infants 14-20g Hgb/100ml
Adult Male 14-15g Hgb
/100ml Female 12-15g
Hgb /100 ml 1.3 ml O2/g Hgb
RBC’s (Light Microscopy)
RBC Physiology RBC specialized for O2
carrying 280 million Hgb
molecules/cell All internal space
available for O2 carrying - no metabolism
Concave shape Allows higher surface
area/volume ratio increases gas diffusion
Allows passage through capillaries, very flexible
RBC Physiology
RBC Physiology
O2 combines with Hgb in lungs O2 not very soluble in H2O Need something to carry it
Hemoglobin 4 globin (protein) chains - 2 chains, 2 chains 4 non-protein heme pigments Heme pigment has iron ion (Fe²+) that carries 1 O2
Each RBC can carry about 1 billion O2 molecules RBC's carry ¼ CO2 bound to hgb - forms
carbaminohemoglobin
RBC Life Cycle Life span
Only 100-120 days Cells cannot repair damage due to loss of nucleus,
ribosomes Old RBC’s destroyed in liver, spleen
Macrophages eat old RBC's Breakdown products recycled Different pathways for each part of Hgb molecule
globin - AA's used for other protein synthesis heme
• iron portion - Fe2+ recycled• non-iron portion - bilirubin
– released in bile, secreted into blood– bile enters intestine converted to urobilinogen by
bacteria– gives urine/feces color
RBC Life Cycle
Granular Leukocytes
Neutrophil
Eosinophil
Basophil
Neutrophil 60-70% of all WBC’s Anatomy
10-12 µm diameter 2-5 connected nuclear
lobes Fine, pale lilac granules
Physiology Respond first to bacteria
damage by chemotaxis Phagocytosis After engulfing pathogen
release several chemicals
lysozymes strong oxidants defensins
Eosinophil 2-4% of all WBC’s Anatomy
10-12 µm diameter 2-3 connected
nuclear lobes red/orange large,
uniform granules, do not block nucleus
Physiology Exit capillaries, enter
tissue fluid Combat
parasites histamine
Phagocytize antigen-antibody complexes
Basophil 0.5-1% of all WBC’s Anatomy
8-10 µm diameter Bilobed nucleus Large granules round,
blue-black, block nucleus
Physiology Exit caps enter tissue
fluids Release heparin,
histamine, serotonin – stimulate inflammation
Hypersensitivity (allergic) reactions
Agranular Leukocytes
Lymphocyte
Monocyte
Lymphocytes
20-25% of all WBC’s
Anatomy 7-15µm Nucleus dark
stained, round or indented
Cytoplasm sky blue rim around nucleus
Lymphocytes - Physiology
Immune response through lymphocytes responding to antigen
An antigen is: Any chemical substance recognized as foreign
when in body Substance (mainly proteins) that stimulate
immune response
Lymphocytes - Physiology
Two types of lymphocytes B-cells
particularly active in killing bacteria develop into plasma cells to form antibodies
• antigen blockers that create antibody-antigen complex
• complex prevents interactions w/ other body cells
T-cells kill viruses, fungi, transplants, cancer, some
bacteria 3 types of cells
• cytotoxic (killer) T cells - destroy foreign invaders • helper T cells - assist B cells and cytotoxic T cells• memory T cells - immune response memory
Monocytes 3-8% of all WBC’s Anatomy
12-20 µm Indented or kidney-
shaped nucleus (not smooth)
cytoplasm foamy Physiology
Slow to respond but arrive in larger numbers
Enlarge, differentiate into wandering macrophages
Clean up cellular debris, microbes following infection
Leukocyte Life Span and Number Life span determined by foreign invaders!
Ingesting foreign bodies toxic, shortens cell life Healthy WBC's - months/years, generally days During infection may only live hours
fill with toxins may die or burst
Leukocyte Life Span and Number 5,000 - 10,000 WBC’s/mm3 blood
RBC/WBC ratio 700/1 Differential WBC count (We have seen these
before!) Neutrophils 60-70% Lymphocytes 20-25% Monocytes 3-8% Eosinophils 2-4% Basophils 0.5-1%
Leukocyte Disorders Leukopenia
Insufficient WBC production Induced by drugs - glucocorticoids, anti-cancer
drugs Leukemia
Cancer (excess production) of the leukocytes Bone marrow fills with cancerous
(nonfunctional) leukocytes Crowds out other cells types
anemia bleeding
Leukocyte Disorders Generally a
descendent of a single cell Different types of
cells myelocytic
leukemia lymphocytic
leukemia Under different
cancerous conditions acute - if derived
from -blast type cells
chronic - if derived from later stages
1.
2.3.
4.
5.Answers
1. Neutrophil2. Basophil3. Monocyte4. Lymphocyte5. Eosinophil
QUIZ!Identify themarked cells!
Platelets - Thrombocytes Development
Megakaryoblasts shed small fragments
Each fragment has plasma membrane
Anatomy 250,000-
400,000/mm3
No nucleus, disc shaped
2-4 µm diameter w/ many granules
Platelets Physiology
Short life span (5-9 days)
Help plug small holes in vessels
Granules several important functions
alpha granules• clotting factors• platelet derived
growth factor (PDGF)
dense granules - Ca++, ADP, ATP, etc.
Also Thromboxane A2, vasoconstrictors, clot promoting enzymes
Hemostasis
3 mechanisms in stopping bleeding
First - Vascular Spasm Blood vessel constricts when damaged
wall smooth muscle contracts immediately slows flow through vessel reflexive?
Hemostasis Second - Platelet Plug
Formation1) Platelet adhesion
platelets stick to exposed collagen activates platelets
2) Platelet release reaction platelets attach to other platelets release granule contents
(thromboxane A2) promote vasoconstriction, platelet
activation and aggregation
3) Platelet aggregation platelet plug blocks blood loss in small vessels not as good in larger vessels
Hemostasis Third -
Coagulation Gel formation
(clotting) in blood traps formed elements
Thrombosis - clotting in a normal vessel
Hemorrhage - slow clotting leading to a bleed
Hemostasis - Coagulation A complicated
process that works in a positive feedback cascade
3 pathways - extrinsic, intrinsic and common
Pathways involve 12 factors in clot formation
Hemostasis - Coagulation
Overview
Stage 1: Prothrombinase formation Prothrombinase
catalyzes Thrombin formation from Prothrombin
Stage 1 has 2 parts Part 1: Extrinsic
Pathway • Rapid (seconds)• Tissue factor
(TF) enters blood from tissue
• Ultimately activates prothrombinase
Hemostasis - Coagulation
Extrinsic PathwayExtrinsic Pathway Intrinsic PathwayIntrinsic Pathway
Prothrombinase
Stage 1: Prothrombinase formation (cont.) Part 2: Intrinsic
Pathway Slower (minutes) Activators in blood -
damaged red blood or endothelial cells activate clotting
Extrinsic pathway also activates Intrinsic pathway
Ultimately activates prothrombinase
Ca2+ required for activation of both paths!
Hemostasis - Coagulation
Extrinsic PathwayExtrinsic Pathway Intrinsic PathwayIntrinsic Pathway
Prothrombinase
Hemostasis - Coagulation Stage 2 - Common
Pathway Thrombin Formation
requires enzyme Prothrombinase w/ Ca++
catalyzes prothrombin conversion to thrombin
Thrombin accelerates formation of prothrombinase (positive feedback)
Thrombin accelerates platelet activation (positive feedback)
Prothrombinase
CommonPathway
+
2.
+
Hemostasis - Coagulation
Stage 3 - Common Pathway Fibrin formation
activated enzyme thrombin w/ Ca++
catalyzes fibrinogen fibrin
• fibrinogen (soluble)• fibrin (insoluble)
Fibrin Protein threads attach to
vessel surface Absorbs/inactivates 90%
of thrombin, limits clot formation
3.
Overview
Hemostasis - Coagulation
Hemostasis - Coagulation
Clot retraction and repair Clot retraction also known as syneresis Platelets continue to pull on fibrin threads
closing wound Formed elements trapped in fibrin threads,
some serum may leak out Hemostatic control mechanisms
Important that clot formation remains local, not systemic
Several mechanisms work together: fibrin absorbing thrombin removal of local clotting factors - washed away endothelial cells inhibit platelet aggregation
Hemostasis - Coagulation Fibrinolysis - dissolution of a
clot, begins within 2 days Plasminogen trapped in clot Many factors convert
plasminogen into plasmin (fibrinolysin)
thrombin activated factor XII tissue plasminogen activator
(t-PA) Plasmin
Digests fibrin threads Inactivates fibrinogen,
prothrombin, and several clotting factors
Hemostasis - Coagulation Thrombolytic (clot-dissolving) agents that can
be used clinically Chemical substances that activate plasminogen Streptokinase, tissue plasminogen activator (t-
PA)
Anticoagulants present in blood - heparin Produced by mast cells, basophils Used clinically to prevent blood clotting in blood
samples Inhibits thrombin and intrinsic pathway
Hemostasis - Coagulation Other anticoagulants
Warfarin (coumadin) - Vitamin K antagonist slow acting, takes days to start and stop rat poison Vitamin K
• produced by gut bacteria• required for synthesis of factors II (prothrombin), VII, IX,
X
Aspirin blocks platelet aggregation prevents formation of thromboxane A2
CPD (citrate phosphate dextrose) removes Ca2+
Used in blood banks
Hemostasis - Coagulation Intravascular Clotting
Roughened endothelium (atherosclerosis, trauma, infection) or slow blood flow may result in spontaneous clot (thrombus) formation, thrombosis
Thrombus released into blood becomes embolus
pulmonary embolus also may be air or debris
Angioplasty - may trigger thrombus
Blood Types
Agglutinins Naturally occurring antibodies produced in response to the
agglutinogens not present in your blood React in antigen-antibody response to blood not of your type
AB - universal recipients O - universal donors
• ABO blood typing– 2 glycolipid agglutinogens, A + B– one gene from each parent, A, B or O– 6 combinations - AA, AB, AO, BB, BO, OO (no agglutinogens)
• RBC surface has genetically determined antigens, agglutinogens
Blood Types
Blood Types Rh typing - Rhesus monkey
With Rh antigens are Rh+
Without Rh agglutinogens Rh-
normally blood does not contain Rh agglutinins
body only makes agglutinins in response to exposure
Rh sensitivity does not occur until second transfusion
hemolytic disease of the newborn
Blood Types Hemolytic
disease of the newborn