University of Baghdad
College of Nursing
Department of Basic Medical Sciences
Overview of
Anatomy and Physioloy –II
Second Year Students
Asaad Ismail Ahmad , Ph.D.
Electrolyte and Mineral Physiology
asaad50.2011@gmail.com
2012 - 2013
ANATOMY AND PHYSIOLOGY - II
Brief Contents
1- Cardiovascular System
2- Blood
3- Lymphatic System
4- Urinary System
5- Male Reproductive System
6- Female Reproductive System
7- Sensory Function
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
Text book
Martini FH. Fundamentals of Anatomy and
Physiology, 5th ed. Prentice Hall, New Jersey,
2001.
References:
1.Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical
Physiology, 23rd ed. McGraw Hill, Boston, 2010.
2.Drake RL, Vogl W, Mitchell AWM. Gray's Anatomy for Students. Elsevier,
Philadelphia, 2005.
3.Goldberger ,E. 1975.A Primer of Water Electrolyte and Acid-Base Syndromes. 5th ed.,
Lea and Febiger ,Philadelphia.
4. Martini, FH and Welch K. Applications Manual Fundamentals of Anatomy and
Physiology,4th ed., Prentice Hall, NewJersey, 1998.
5.Maxwell, MH and Kleeman CR. 1980.Clinical Disorders of Fluid and
Electrolyte Metabolism. McGraw-Hill Book Company, New York.
6.McKinley M, and O'Loughlin VD. Human Anatomy, McGraw Hill, Boston,
2006.
7.Nutrition Foundation.1984.Present Knowledge in Nutrition. 5th ed.,
Nutrition Foundation, Inc , Washington, D.C.
8.Vander A, Sherman J, Luciano D., Human Physiology, 7th ed., McGraw Hill,
Boston, 1998.
BLOOD
Contents:
BLOOD
1- Overview of the blood.
2. Functions of the Blood.
3. Plasma
4. Erythrocytes (Red Blood Cells).
5. Leukocytes (White Blood Cells).
6. Platelets (Thrombocytes).
7. Hemopiesis (Hematopoiesis).
8. Hemostasis.
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
SIXTH LECTURE
Blood
6. Platelets (Thrombocytes).
7. Hemopoiesis (Hematopoiesis).
8. Hemostasis.
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
CONTENTS:
6. Platelets (Thrombocytes).
Continue: Overview PLATELETS
1234-
Small fragments of megakaryocyte cytoplasm
2-4 um diameter, contain granules
Rather than individual cells, it is flattened disc, round.
Each platelet circulate in the bloodstream for 9-12
days, before being removed by phagocyte.
5- Normal count: 130,000 – 400,000 ul
FUNCTION:
1- Secrete clotting factors and growth factors for vessels repair
2- Initiate formation of clot dissolving enzyme
Platelets Production (Thrombocytopoiesis):
Megakaryocytes in bone marrow manufacture
Structural proteins, enzymes, and membrane.
They shade cytoplasm in small membrane
enclosed packet. These packets are platelets.
A mature megakaryocyte produce 4000 platelets
platelets
Onions & Low Platelet Count
Onions contain a chemical that is known to reduce platelet activity in
humans and dogs.
Continue:
Hemopoiesis
(Hematopoiesis)
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
HEMOPOIESIS (HEMATOPOIESIS):
PRODUCTION OF FORMED ELEMENTS
Hemopoiesis occurs in red bone marrow. The
Process of hemopoiesis starts with hemopoietic
Stem cells called Hemocytoblasts, which consider
Pluripotent cells. Hemocytoblasts differentiate
Into many different kinds of cells. Hemocytoblasts
produce two lines for blood cell development:
1- Myeloid (line) Stem Cells forms erythrocytes,
Megakaryocytes and all leukocytes except
Lymphocytes.
2- Lymphoid (line) Stem Cells forms lymphocytes.
Production of blood cells by the bone marrow
TYPES OF HEMOPOIESIS (HEMATOPOIESIS)
Hematopoiesis: Blood cells formation
and differentiation in bone marrow
TYPES OF HEMOPOIESIS
1- Erythropoiesis : Red blood cell formation
inbone marrow.
2- Leukopoiesis : White blood cell formation.
3- Lymphopoiesis: Production of lymphocytes
from lymphoid stem cells.
4- Thrombocytopoiesis: Platelets production.
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
FACTORS REGULATE ERYTHROPOIESIS
(RBCs PRODUCTION)
1- Erythropoietin (EPO): hormone secreted
by kidneys.
2- Hormone: thyroxin, androgen, cortisol.
3- Vitamin: B12, B6, Folic acid, vitamin C
4- Amino acids: for synthesis hemoglobin.
5- Metals: iron, cobalt and manganese.
FACTOR REGULATE THROMBOCYTOPOIESIS
1- Thrombopoietin: hormone produce by kidneys
FACTORS REGULATE LEUKOPOIESIS
(WBCs PRODUCTION)
1- Multi-CSF: granulocyte, monocyte, platelets,
RBCs colony stimulating factor.
2- GM-CSF: granulocyte, monocyte colony S.factor
3- G-CSF : granulocyte colony stimulating factor.
4- M-CSF : monocyte colony stimulating factor.
5- Thymosin: hormone produce by thymus
stimulate T- lymphocyte maturation and
B- lymphocyte production.
6- Antigens: exposure to antigens promote the
production of lymphocytes, B-cells and T-cells
Note: the 1st, 2nd, 3rd and 4th factors are secreted
by lymphocytes.
CONTENTS:
HEMOSTASIS
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
HEMOSTASIS 645
(positive feedback control of blood clotting)
Hemostasis: stopping the bleeding through
the wall of damage vessels, by clot
formation or vessel spasm.
The processes (steps)of
hemostasis are:
1- Vascular phase
2- Platelets phase
3- Coagulation phase
HEMOSTASIS:
1– VASCULAR PHASE
Vascular phase lasts about 30 minutes, start
When the wall of blood vessels is cutting.
During this phase the following changes occurs:
1- Vascular spasm: contraction of local smoth
Muscle fibers of the vessel wall.
2- Releasing chemical factors (mediators): (prostacyclin,
nitric oxide) and local hormones (endothelins), by
endothelial cells.
3- Endothelium cell membrane become sticky:
On opposite side of the vessel endothelial cells
Stick together.
2- PLATELET PHASE (PLATELET PLUG)
Platelet phase start when the platelets attached
to sticky endothelial surface. This process
Called platelets aggregation forming platelets
plug . This begins within “15 second” after injury
(damage). When the platelets arrive injury site it
becomes Activated and begin to releasing:
1- ADP “adenosine Diphosphate”
2- Thromboxane A2
3- Serotonin
4- Clotting factors
5- platelets growth factor
6- Calcium ions “ Ca++”
3- COAGULATION PHASE
(formation of blood clot) 647
Cagulative phase dose not start until 30 seconds
after the vessel has been damaged. Coagulation
or formation of blood clotting involve complex
process leading to conversion of soluble circulating
Fibrinogen into the insoluble protein fibrin. As the
fibrin network grows, it covers the surface of platelet
Plug. Passing blood and additional platelets are
trapped in the fibrous tangle, forming a blood
clot, which effectively seals off the damaged
portion of the vessel
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
BLOOD CLOT
BLOOD CLOT
BLOOD CLOT
CLOTTING FACTORS 648
I- Fibrinogen
II- Prothrombin(vit.k)
III- Tissue factor
IV- Calcium ions(Ca++)
V- Proaccelerin
VI no longer used
VII-Proconvert (vit.k)
VIII-Antihemophilic
IX- Plasma
thromboplastin (vit.k)
X- Stuart-power factor
(vit.k)
XI- Plasma
thromboplastin
XII- Hageman factor
XIII- Fibrin-stabilizing
NEGATIVE FEEDBACK CONTROL OF BLOOD CLOTTING (
regulation of clotting mechanisms )
1- Heparin: release by basophil and mast cells,
activate antithrombin III. Heparin used clinically
to prevent clotting.
2- Thrombomodulin: protein release by
endothelial cells, bind to thrombin and convert it
to enzyme activate protein C, then protein C
inactivate several clotting factors and stimulate
formation of plasmin, the enzyme that gradually
breaks down fibrin strands.
Continue: NEGATIVE FEEDBACK CONTROL OF BLOOD
CLOTTING
3- Prostacyclin and Nitric oxide: release by
normal intact endothelial cells, to maintain
resting platelets and inhibit platelets
aggregation and opposes the action of thrombin,
ADP, and other clotting factors.
4- Alpha-2-macroglobulin: plasma protein inhibit
thrombin and several clotting factors.
5- Magnesium ions (Mg++): is anticoagulant
factor.
Continue: NEGATIVE FEEDBACK CONTROL OF BLOOD
CLOTTING
6- Antithrombin, proteins C & S
These proteins are the body’s natural anticoagulants,
hence deficiencies may lead to thromboembolic disease
Factors Decrease Antithrombin ( AT levels )
1- Hereditary (40–60% normal level), autosomal dominant.
2- Chronic liver disease.
3- Protein wasting disorders.
4- Heparin therapy.
5- 3rd trimester of pregnancy.
6- Acute leukaemia.
7- Burns.
8- Renal disease.
9- Gram –ve sepsis.
CLOTTING RETRACTION AND FIBRINOLYSIS
Fibrinolysis: process of dissolving clot.
1- Activation of proenzyme” plasminogen” by;
a- Thrombin
b- Tissue plasminogen activator
2- Plasminogen change to plasmin. Plasmin is the
enzyme which digesting and eroding the clot.
Note: clot retraction occurs within 30-60
minutes
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
HEMOSTASIS DISORDERS
I- Inadequate blood clotting
1- Hemophilia
a- Hemophilia type A - deficiency factor 8
b- Hemophilia type B - deficiency factor 9
c- Hemophilia type C - deficiency factor 11
II- Excessive blood clotting
1- Thrombosis: formation of thrombus
Thrombus : blood clot attached to vessel wall
2- Embolism: blood clot, fat globule, air or
bubble circulating in the blood.
3- Infarction
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology