erythroblastosis fetalis (hemolytic disease of the newborn)

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Blood: The River of Life
Blood
• Two components
– Formed elements
• Leukocytes (WBC) and platelets (buffy coat)
equal less than 1% of blood
• Erythrocytes (RBC) equal 45% of blood
– Hematocrit = measure of RBC present
– Plasma (fluid portion) = 55% of blood
Blood Information
• pH = 7.35 – 7.45
• Temperature = 38oC or 100.4oF
– Slightly higher than body temp.
• Approx. 8% of body weight
– Males have 5-6 L while females have 4-5 L
although amount depends on size
• Color
– Oxygen rich blood is scarlet red
– Oxygen poor blood is dull or rusty red
– Blood is heavier & more viscous than water
Functions of Blood
• Transport:
Respiratory gases, hormones, cells and
compounds
• Maintenance
Normal pH, Adequate fluid volume,
electrolyte balance
Functions of Blood
• Prevention:
– Blood loss through damaged vessels
/clotting mechanisms
• Defense:
- Against pathogens using WBC and to
help eliminate toxins
• Absorb, distribute heat as part of
temperature regulation.
*overall helps with maintaining the
organisms homeostasis.
Erythrocytes
• Structure:
– Anucleate
• Only survive ~120 days
– Few organelles
– Lack mitochondria
• Don’t do aerobic respiration so don’t use up the
oxygen that they are carrying
– Biconcave shape
• Allows for more surface area for diffusion of
gases to take place
RBC Proteins
• Hemoglobin
– 33% of cell weight
– Carries oxygen on
iron atoms
RBC Proteins
• Spectrin
– Adds flexibility so cell can change shape
without rupturing as it squeezes through
capillaries
• Misc. other proteins help with facilitating
gas exchange and other functions
RBC proteins
Numbers of RBCs
• Outnumber WBC 1000 to 1
• Women
– 4.3 – 5.2 million RBC per mm3 of blood (about 1
small drop)
• Men
– 5.1 – 5.8 million RBC per mm3 of blood
• # of blood cells compared to amount of
plasma is major factor in blood viscousity
– If blood is too viscous – heart must work too hard
to pump it
Anemia vs. Polycythemia
Functions of RBCs
• Major function is to carry oxygen
• Single RBC contains ~250 million
hemoglobin
molecules each
capable of carrying
4 oxygen atoms
Hemoglobin
• Values
– Infant: 14-20 g / 100 ml
– Male: 14-18 g / 100 ml
– Female: 12-16 g / 100 ml
• Protection of hemoglobin
– Enclosed in RBC to prevent fragmentation
which would increase blood viscosity
Hemoglobin
• Oxyhemoglobin
– With O2 = bright scarlet red
• Deoxyhemoglobin
– W/o O2 = dull/rusty/dark red
• Carbaminohemoglobin
– With CO2
• Carboxyhemoglobin
– With CO
Hematopoiesis
• Blood cell formation
– Occurs in red bone marrow which is found
in the ends of long bones and in flat bones
• Hemocytoblasts convert to hemocytes
– Cycle takes 3-5 days
Stem Cells
Erythropoiesis
Red blood cell formation
– Based on oxygen demands
• Hypoxia: too few = oxygen deprivation
• Too many (polycythemia) = increased blood viscosity *Two
main types of polycythemia• Primary is inherited/congenital (incurable but treatable)
Secondary is due to exposure to smoke, exposure to
carbon monoxide & other risk factors HBP, Diabetes.
• Hyperviscosity syndrome
– Average production rate = 2 million/sec
– Controlled hormonally
• Based on level of available oxygen
• Renal erythropoietic factor triggers erythropoietin production
in kidney
Erythropoiesis
Erythropoiesis
• Production depends on:
– Fe, B12 vitamin, and folic acid
• Necessary for DNA synthesis and hemoglobin
synthesis
• Small amounts are lost daily in feces, urine,
sweat, and menstrual flow
– 65% (4000mg) of iron stored is in
hemoglobin
– Free elemental iron is TOXIC so:
• Iron is stored as ferritin or hemosiderin
• Iron is transferred in the blood as transferrin
Life Cycle of RBCs
• After 120 days, the RBC is degraded
and recycled
• Hemoglobin is broken down to bilirubin
– Goes to liver to be excreted
– Liver damage can cause jaundice affecting
many body organs
– Bilirubin excess in brain causes kernicturus
Life Cycle of RBCs
Side Note:
• Cancer of WBC – Leukemia
Ex. Specifically “B” lymphocytes cancer is
known as Waldenstrom’s Macroglobulinemia
• Cancer of RBC – Multiple Myeloma
Different ones affecting the different
myeloid stem cells
Leukocytes (WBCs) – body defense
system
• 4000 – 11,000 per mm3
• Complete cells with nuclei and various
organelles
Leukocyte Features
• Diapedesis
– Reach infection site by slipping into and
out of blood vessels
• Ameboid motion
– Move through tissue spaces to reach
location
• Chemotaxis
– Respond to chemicals released by
damaged cells in order to locate damaged
area
Leukocytes-Granulocytes
• Neutrophils
• Basophils
• Eosinophils
Leukocytes
• Know the features and function of each type of WBC:
see notes
• Granulocytes – contain specialized granules and
lobed nuclei
– Neutrophils
• Most numerous
• Active phagocytes – attracted to inflammation through
chemotaxis
• Numbers increase during bacterial & fungal infections
• Produce white/yellow pus and snot
– Basophils
• Least numerous
• Located in certain tissues – aka. Mast cells
• Produce heparin & histamine to cause vasodilation and attract
other WBCx to area of attack
• Produce clear watery snot
Leukocytes con’t
• Eosinophils
– 1-4% of WBCs
– Located in intestinal & pulmonary mucosa
and in dermis
– Increase in number during
• Parasitic worm infestations
• Protozoal infestations
• At end of allergy attack – produce chemicals to
counteract allergic reactions
• Produce greenish snot
Leukocytes-Agranulocytes
• Lymphocytes
• Monocytes
Leukocytes
• Lack granules
• Formed in bone marrow and then
migrate to lymphatic tissues – rarely
circulate in blood unless needed
• 2 types
Leukocytes
• Lymphocytes
– 2nd most numerous WBC – 20 to 40%
– Play an immune system role
• T-cells (several types)
– Attack virus infected & tumor cells
• B-cells (several types)
– Produce antibodies (immunoglobulins)
Leukocytes
• Monocytes
– Largest of WBCs
– Very mobile, aggressive macrophages
– Increase in number during chronic
infections (such as tuberculosis) and act
against viruses and bacteria in long term
infections
– Activate lymphocytes to start immune
response
Leukopoiesis
• CSFs and interleukins stimulate
•
•
•
•
production
Activated in response to infections,
toxins, tumor cells, etc.
Granulocytes produced and stored in
bone marrow as needed
Granulocytes have short life span – die
fighting invaders
Agranulocytes may live days to years
depending on type
Plasma
•
•
•
•
Straw colored, sticky fluid matrix
90% water
10% dissolved proteins, gases, wastes, etc.
Plasma proteins produced by liver: know
functions:
–
–
–
–
Albumin
Fibrinogen
Alpha & beta globulins
Gamma globulins
• Homeostatic levels maintained by various
organs
Platelets (Thrombocytes)
• Formed by megakaryocytes (stem cells)
• Fragments of cells that clump together
to form a seal at damaged BV locations
• Not a complete cell – lack nuclei and
organelles so short life span
Clot formation
Blood Volume Worksheet
• Quickly complete the calculations on
your Blood Volume Worksheet
– Measure out the amounts using the
colored water
Steps of Hemostasis
• Platelet plug formation
– Normally, platelets and endothelium are both
positively charged so they repel each other and
the endothelial wall of BV
– When endothelium ruptured, +platelets contact
negative collagen fibers
– Chemical changes cause platelets to swell and
stick together and to the wall
– Chemicals are released to attract more platelets to
seal cuts
– Platelet plug is formed – effective in sealing small
vascular nicks
Aspirin
• Aspirin inhibits platelet plug formation
and prolonged bleeding may occur
– In small doses, it inhibits unecessary
clotting thus preventing heart attacks &
strokes
• Aspirin is an anticoagulant
Steps to Hemostasis
• Vascular Spasms
– Pain and serotonin release triggers
vasoconstriction
– More efficient when crushed than when it is
a clean cut
Steps to Hemostasis
• Coagulation – blood clotting
• Critical events that occur:
– Thromboplastin released by injured tissue
– interacts with prothrombin activator (PF3)
– Which converts prothrombin to thrombin
– Which joins fibrinogen molecules into a
fibrin mesh
– Which traps RBCs and pulls edges closer
together
Hemostasis (blood stopping)
Hemostasis
• More than 30 substances involved
– Procoagulant – promotes clotting
– Anticoagulant – inhibits clotting
• Pathways
– Intrinsic
• Thromboplastin comes from platelets
• 3-6 minutes for pathway
– Extrinsic
• Thromboplastin comes from injured tissue
• 15 seconds for pathway
Fibrinolysis (clot busting)
Fibrinolysis
• When normal cell regeneration begins,
clot becomes unnecessary
• Plasmin (clot buster) is released until
clot is dissolved totally
Factors that limit Clot formation
• Dilution of factor
– Normal blood flow keeps factors diluted
• Impairment
– Heparin in blood inhibits any clotting
factors that have been activated but not
used
– See imbalance symbol page 586
• Molecular
– Structural & molecular characteristics of
endothelium & platelets
Disorders of Hemostasis
• Type I: Thromboembolytic conditions –
undesirable clot formation
– Thrombus: clot that develops in an
unbroken blood vessel
– Embolus: thrombus that breaks away from
BV wall and floats freely in bloodstream
• Either may block circulation to tissues beyond
the occlusion and cause death to those tissues
• Pulmonary embolism, stroke, heart attack
Disorders of Hemostasis
• Endothelial roughening: impairment of
endothelial characteristics such as
arteriosclerosis, severe burns/scar tissue, or
inflammation may give platelets a place to
cling and begin a thrombus
• Blood stasis: slowing of blood flow
particularly in immobilized patients does not
keep clotting factors diluted
Disorders of Hemostasis
• Bleeding disorders: prevention of
proper clot formation
– Thrombocytopenia: platelet count under
50,000 per mm3
• Petechiae: small purplish blotches (bruises)
caused by spontaneous bleeding from small BV
all over body
• Cause: damage to myeloid tissue (bone
marrow): bone marrow cancer, radiation,
certain drugs
• Treatment: whole blood transfusion or in some
cases platelet transfusion
Disorders of Hemostasis
• Impaired liver function
– Little to no procoagulants produced
– Causes: vitamin K deficiency, hepatitis,
cirrhosis
• Vitamin K is a fat soluble vitamin produced in
your intestines by bacteria: liver produces bile
which is necessary for fat absorption
– No bile = no fat absorption = vitamin K deficiency =
no procoagulant production
– Treatment: Depends on cause
Hemophilia
• Hereditary X linked trait so usually affects
males
– Hemophilia A = factor VIII deficiency – most
common
– Hemophilia B – factor IX deficiency
– Hemophilia C – factor XI deficiency
• Symptoms: minor tissue trauma causes
prolonged bleeding, bleeding into joint
capsules after exercise or trauma
• Management: clotting factor transfusion
RBC & WBC disorders
• See notes
Blood Groups
• RBCs contain antigens (glycoproteins) for cell
recognition
– 30 common varieties - over 100 "family antigens"
– common antigens - ABO and Rh cause vigorous transfusion
reactions
– others mainly used for ID purposes (paternity, inheritance,
etc. - only typed in cases of several transfusions (cumulative
effect)
• ABO blood groups
– based on presence or absence of A or B antigens
on RBCs
– plasma antibodies act against antigens not
present on that individual's RBCs
– see chart
Antigens & Antibodies
Rh factor
• Rh+ 85% of Americans - carry Rh antigen on RBC
• Rh- don't have antigen on RBC
• less severe transfusion reaction (hemolysis of donor
RBCs) - doesn't usually occur until 2nd transfusion
due to body's reaction time
• can cause erythroblastosis fetalis (hemolytic
disease of the newborn) if Rh- woman carries Rh+
baby
– 1st baby is usually okay due to reaction time unless there
was a bleeding problem during the pregnancy or a previous
miscarriage or abortion.
– 2nd baby will have its blood cells attacked by mother’s
antibodies– Rhogam shot can prevent this if injected at 28 weeks of
pregnancy and again right after birth.
Transfusions
• In case of blood loss, body tries to:
– 1. reduce BV volume to maintain circulation to vital organs
– 2. step up production of RBCs for replacement
•
•
•
•
15-30% loss - pallor & weakness
over 30% - severe shock may be fatal
substantial blood loss - whole blood transfusion
Plasma, electrolyte solutions ( Ringer's solution) etc.
can be used to increase blood volume while body
steps up production of RBCs
Transfusion Reaction
• Mismatched RBCs antigens attacked by
plasma antibodies
• agglutination of foreign RBCs can:
– clog small BV - reduce blood flow
– lysed RBCs release hemoglobin into bloodreduced oxygen capacity - blocks kidney tubules
and causes renal shutdown
• Reactions: fever, chills, vomiting
• Treatment: alkaline fluids to dilute
hemoglobin, diuretics to increase urine flow to
flush kidneys
Agglutination
Know the information contained in
this chart
Developmental Aspects
• Embryonic
– Day 28 of pregnancy – RBC in fetal
circulation
– By 7th month: red marrow is chief site of
hematopoiesis
– HbF – fetal hemoglobin
• Greater ability to pick up oxygen
• Replaced by HbA after birth
• Immature liver may lead to physiological
jaundice
Developmental Aspects
• Adulthood
– Dietary deficiencies or metabolic disorders
cause abnormalities in BC formation or
hemoglobin production
– Iron deficient anemia more common in
women
Developmental Aspects
• Old age
– Leukemia risk
– Pernicious anemia
• Stomach mucosa atrophies with age
• Less intrinsic factor (located in lining of
stomach – function is B12 absorption)
• Less B12 absorption
• Leads to pernicious anemia
Diagnostic Blood Tests
•
•
•
•
•
•
low hematocrit = anemia
high fat level (lipidemia) = problems with heart
disease
blood glucose test – diabetes, hypoglycemia,
hyperglycemia
differential WBC indicates type of infection
platelet count – thrombocytopenia – clotting
problems
complete blood count = CBC – see handout
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