notes

Report
Chapter 17a
Circulation
Characteristics of Blood
RBC and Erythropoiesis
Overview of Vessels
Arteries: blood
vessels that move
AWAY from the
heart
Veins: vessels that
move TOWARD the
heart
Capillaries: Small vessels
created by repeated
branching of arteries and
veins
• 1 epithelial cell layer thick
• allows for gas, waste, and
nutrient exchange at the
tissue level
Blood Circulation
6. CO2 and waste move from tissues into
vessels
1. O2 deficient blood moves into veins
that enter the right atrium of heart
2. Right ventricle
pumps blood through
the pulmonary artery,
which carries blood to
lungs, where it
releases CO2 and
picks up O2
3. O2 rich blood returns to the
heart via pulmonary veins and
enters left atrium of heart
5. O2 and nutrients diffuse across
capillary walls into tissues
4. Blood leaves left
ventricle of the heart
via aorta and moves
into arteries towards
tissues
Heart Anatomy
(pump your blood song)
Pulmonary Valve
= R Semi-lunar Valve
R Atrioventricular valve
= Tricuspid valve
Aortic Valve
= L Semi-lunar Valve
L Atrioventricular
valve
= Mitral Valve
= Bicuspid Valve
Heart Valves
(Cross Section; Inferior View)
Physical Characteristics of Blood
•
•
•
•
•
•
•
Body’s only fluid tissue
Sticky plasma
Color: scarlet (O2 rich) to dark red (O2 poor)
pH: 7.35–7.45 (slightly basic)
Temperature: 38C (100.4F)
8% of total body weight
AVG volume:
– males: 5 - 6 L
– females: 4 - 5 L
Functions of Blood
1. Distribution: Transportation of
– Oxygen from lungs to cells
– Nutrients from intestines to cells
– Metabolic wastes from cells to lungs and kidneys
for elimination
– Hormones from endocrine glands to target organs
Functions of Blood
2. Regulation: Maintenance of
– Body temperature
– pH with buffer proteins and solutes
• pH imbalances interfere w/ cell activities, causing tissue
damage
– Fluid volume
Functions of Blood
3. Protection:
a. Fights infections
– Synthesizing and
employing antibodies
– Activating complement
proteins
– Activating WBCs to
destroy foreign invaders
Functions of Blood
3. Protection:
b. Prevention of blood loss by
– Activating plasma proteins and platelets
– Initiating clot formation when a vessel is broken
Composition of Blood
• Composed of liquid plasma (matrix) and
formed elements (cellular)
Composition of Blood
• Hematocrit = % of RBCs out of total blood
volume
Males: 47%
Females: 45%
Blood Plasma
• 90% water by volume
• > 100 solutes, including:
1. Proteins
• Albumin (liver protein):
– blood buffer; maintains osmotic pressure
• Globulins:
– α, β (liver proteins) : transport lipids, metal ions, fatsoluble vitamins
– Gamma ɣ: antibodies during immune response
• Fibrinogen: clotting protein
Blood Plasma
• 90% water by volume
• > 100 solutes, including:
2. Lactic acid, urea, creatine
3. Hormones: ex. insulin, erythropoietin, and others
4. Organic nutrients: carbohydrates, amino acids,
lipids
5. Electrolytes: Na+, K+, CA2+, Cl-, bicarbonate (HCO3),
etc.
6. Respiratory gases: O2 and CO2
Formed Elements
• Erythrocytes (RBC), leukocytes (WBC), and platelets
(for clotting)
• Only WBCs are complete cells
– RBCs have no nuclei or organelles
– platelets are just cell fragments
• Most survive in the bloodstream for only a few days
(RBC: 100 – 120 days)
• Most are amitotic (do not divide)
– replaced by stem cells in bone marrow
Components of Formed Blood
Erythrocyte (RBC) Characteristics
• Biconcave discs  High SA/V ratio (> 30% than spherical)
• Contributes to blood’s viscosity
• anucleate (no nucleus), and no organelles, no mitochondria
 anaerobic ATP generation; do not use any O2 that
they transport
• Contain spectrin
membrane protein on
cytoplasmic face
 Flexibility
 Ability to change shape
 Ease of movement through
narrow capillaries
Gas Transport
• RBCs with > 97% hemoglobin (Hb)
 protein used for transport of O2 and CO2
• Binding Hb to CO arrests cellular respiration
Hemoglobin (Hb) Structure
• 4 Globin proteins, each globin bound to a heme group
• Heme = red pigment w/ an atom of iron (Fe)
 binds to O2 and changes to scarlet red
Fun Fact:
• 1 Hb can
transport 4 O2
molecules
• One RBC has
250 million Hb
molecules
• The cell
transports 1
billion
molecules of
O2!
Forms of Hb
• Oxyhemoglobin – Hb bound to oxygen O2
– O2 loading happens in the lungs
• Deoxyhemoglobin – Hb after O2 diffuses into tissues
• Carbaminohemoglobin – Hb bound to CO2
– CO2 loading happens in the tissues
How does loading and unloading of respiratory gasses
happen? Watch this video and take notes to find out…
Hematopoiesis
• Blood Cell Formation
• Occurs in red bone marrow of:
– Axial skeleton and girdles
– Epiphyses of the humerus and femur
• Hemocytoblasts (adult stem
cells of blood):
- give rise to all formed
elements
• Erythropoeisis: specific
formation of RBC
Erythropoiesis
Developmental Pathway
• Phase 1: Ribosome synthesis for globulin protein formation
• Phase 2: Hemoglobin accumulates
• Phase 3: Nucleus and Organelles eject
 Reticulocytes: still w/ remnants of RER and ribosomes
 Erythrocytes: complete RBC, all ribosomes degraded by
enzymes
Fun Fact: process takes 15 days; 2 million RBCs made/minute
Dietary Needs
1. Iron (Fe)
• 65% of Fe in body is in Hb
• Remainder stored in liver, spleen, marrow as protein-iron
complexes: ferritin and hemosiderin
– free iron ions Fe2+ and Fe3+ are toxic, increasing free radicals, causing cell
death
2. vitamin B12 and folic acid
• For normal DNA synthesis
3. Lipids, CHO, Amino Acids
Iron lost daily via waste
• 0.9 mg/day lost by men
• 1.7 mg by women (menstrual bleeding)
Control of Erythropoiesis
• Delicate balance btw RBC formation and
destruction
– Too few RBC hypoxia (lack of O2 in tissues)
– Too many RBC  blood is too viscous
• Hormonal Controls
– Erythropoietin (EPO):
• hormone made by kidneys
• directly stimulates RBC formation
– EPO released in response to:
• Tissue hypoxia
• Increased tissue demand for O2
EPO Mechanism
Start
Homeostasis: Normal blood oxygen levels
Increases
O2-carrying
ability of blood
Stimulus: Hypoxia due to
decreased RBC count,
decreased amount of
hemoglobin, or decreased
availability of O2
Reduces O2 levels
in blood
Enhanced
erythropoiesis
increases
RBC count
Erythropoietin
stimulates red
bone marrow
Kidney (and liver to a smaller
extent) releases erythropoietin
Fate of Erythrocytes
• RBC w/ no nuclei, no DNA, no new proteins
Fragile, lose shape, becomes rigid
Hb degenerate
• RBCs often trapped and
fragmented in spleen
• Dying RBC engulfed and
destroyed by
macrophages
• Components of Hb are
broken down and some
parts recycled for reuse.
Life Cycle of Erythrocytes
Low O2 levels in blood stimulate
kidneys to produce erythropoietin.
Erythropoietin levels
rise in blood.
Erythropoietin and necessary
raw materials in blood promote
erythropoiesis in red bone marrow.
Aged and damaged red
blood cells are engulfed by
macrophages of liver, spleen,
and bone marrow; the hemoglobin
is broken down.
Hemoglobin
New erythrocytes
enter bloodstream;
function about
120 days.
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
Globin
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
Globin
Amino
acids
2. Globin metabolized
into AA and released
into blood
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
3. Heme degraded into
yellow pigment Bilirubin
Globin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
2. Globin metabolized
into AA and released
into blood
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
3. Heme degaded into
yellow pigment Bilirubin
4. Iron stored safely as
ferritin and hemosiderin in
liver
Globin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
2. Globin metabolized
into AA and released
into blood
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
3. Heme degaded into
yellow pigment Bilirubin
4. Iron stored safely as
ferritin and hemosiderin in
liver
Globin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
5. Iron is bound to
transferrin protein and
released into
circulation
for erythropoiesis
2. Globin metabolized
into AA and released
into blood
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
3. Heme degaded into
yellow pigment Bilirubin
4. Iron stored safely as
ferritin and hemosiderin in
liver
6. The liver secretes
bilirubin into intestine with
bile from the gall bladder
7. The intestines
metabolize it, and it leaves
the body in feces as a
pigment called stercobilin
(brown poop)
Globin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
5. Iron is bound to
transferrin protein and
released into
circulation
for erythropoiesis
Bilirubin is
metabolized by
intestines and
excreted in feces
2. Globin metabolized
into AA and released
into blood
Destruction of Hb
1. Heme and Globin
separated
Hemoglobin
Heme
Bilirubin
3. Heme degaded into
yellow pigment Bilirubin
Iron stored
as ferritin,
hemosiderin
4. Iron stored safely as
ferritin and hemosiderin in
liver
6. The liver secretes
bilirubin into intestine with
bile from the gall bladder
Globin
Amino
acids
2. Globin metabolized
into AA and released
into blood
5. Iron is bound to
transferrin protein and
released into
circulation
for erythropoiesis
Bilirubin is
metabolized by
intestines and
excreted in feces
7. The intestines
metabolize it, and it leaves
the body in feces as a
Food nutrients,
pigment called stercobilin including amino
acids, Fe, B ,
(brown poop)
and folic acid
Circulation
12
are absorbed
from intestine
and enter blood
8. Raw materials are made available in
blood for erythrocyte synthesis.
Erythrocyte Disorders
1. Polycythemia – excess RBCs that increase blood
viscosity
• Causes clotting in small capillaries, leading to
– Stroke
– Heart Attack
• 3 types:
– Polycythemia vera: bone marrow disease
– 20 polycythemia: people living at high altitudes.
– Blood doping : enhancing RBC numbers to increase
athletic performance
• removing blood for a few days, then re-infusing it.
Erythrocyte Disorders
2. Anemia – blood has abnormally low oxygencarrying capacity
• Symptom; not a disease
• Blood oxygen levels cannot support normal
metabolism
• Causes fatigue, paleness, shortness of breath,
chills
Anemia: Insufficient Erythrocytes
• Hemorrhagic anemia: due to acute or chronic
loss of blood (ex. stab wounds)
• Hemolytic anemia: RBCs prematurely
destroyed (ex. abnormal proteins of RBCs,
abnormal immune system, parasitic)
• Aplastic anemia: bone marrow failure: does
not produce enough RBCs
Anemia: Decreased Hb Content
• Iron-deficiency anemia results from:
– hemorrhagic anemia
– Poor diet: lack of iron-containing foods
– Impaired iron absorption
• Pernicious anemia results from:
– Inability to absorb vitamin B12
• Not enough intrinsic factor (protein that aids in B12
absorption)
Anemia: Abnormal Hemoglobin
• Thalassemias – absent or faulty globin chain in Hb
– RBCs are thin, delicate, and deficient in Hb
– Can lead to hemolytic anemia
• Sickle-cell anemia – from abnormal Hb-S
– Hb-S due to genetic mutation of a single amino
acid (substitution), causing sickle-shape of RBC
• Both conditions offered some protection from
malaria

similar documents