Functions of the blood
Transport oxygen and nutrients for cell metabolism
Removal of cellular waste
Maintains homeostasis
Tunica intima
Endothelial layer (inner layer)
Tunica media
Layer of smooth muscle that controls the diameter of the blood vessel (middle layer)
Tunica Adventita
Outer CT layer and contains elastic and collagen fibers
Vasa Vasorum
Tiny blood vessels that supply blood to thewalls of arteries and veins
pH of blood
7.35-.45
How many liters of blood does the adult body contain
5
Hematocrit
Proportion of cells in blood (indicates viscosity)
Plasma
Clear yellowish fluid remaining after cells have been removed
Serum
Fluid and solutes remaining after cells and fibrinogen have been removed
Where do blood cells originate?
Red bone marrow
Dyscrasia
Disorders involving cellular components of blood
Erythrocytes
Biconcave, flexible discs that are non-nucleated when mature and contain hemoglobin
Erythropoietin
A hormone originating from kidneys that stimulate production of erythrocytes in red bone marrow in response to hypoxia
Hemoglobin consists of
Globin, two pairs of amino acid chains, four heme groups which contain iron atoms which oxygen can attach
Oxyhemglobin
Bright red; oxygenated
Deoxyhemoglobin
Dark or bluish red color and is found in venous blood
5 types of WBCs
Lymphocytes Neutrophils Basophils Eosinophils Monocytes
Lymphocytes
B and T lympocytes significant in the immune response
Neutrophils
Most common leukocytes. First response to any tissue damage and commence phagocytosis. Increase in numbers during bacterial infection
Basophils
Migrate from blood and enter tissue to become mast cells that can release histamine and heparin
Eosinophils
Combat the effects of histamine. Increased during allergic reactions and parasitic infections
Monocytes
Can enter tissue to become macrophages, which act as phagocytes when tissue damage occur
Thrombocytes
Also known as platelets
Not cells; small, irregularly shaped, non-nucleated fragments from large megakayocytes
Heparin
An anticoagulant that is released from basophils (or mast cells) in the tissues and exerts its major action by blocking thrombin. It does not dissolve clots, but will prevent further growth of the thrombus
O blood
No antigens
Anti-A and Anti-B antibodies
A blood
A antigens
Anti-B antibodies
B blood
B antigens
Anti-A antibodies
AB Blood
A and B antigens
No antibodies
Complete blood count (CBC)
Total red blood cells, white blood cells,and platelets
Leukocytosis
Increased WBCs
Associated with infection and inflammation
Leukopenia
Decreased WBCs
Associated with some viral infections, radiation, chemotherapy
Increased eosinophils
Common in allergic response
Reticulocyte count
Assessment of bone marrow function
Prothrombin time and partial thromboplastin time
Measures function of various factors in coagulation process
Underlying cause of anemias
Reduction in oxygen transport in the blood due to a decrease in hemoglobin content
Signs and symptoms of anemia
Fatigue, pallor, dyspnea, tachycardia, and high blood pressure
Causes of iron deficiency anemia
Dietary intake of iron below minimum requirement
Chronic blood loss
Impaired duodenal absorption of iron
Severe liver disease
Iron deficiency anemia most common in…
women of childbearing age and pregnant women
Pernicious Anemia
Lack of absorption of vitamin b12 because of lack of intrinsic factor (secreted by gastric mucosa and required for intenstinal absorption of b12)
Pernicious Anemia characterized by
Very large, immature nucleated erythrocytes that carry less hemoglobin and have a shorter lifespan
s/s of pernicious anemia
Tongue is enlarged, red, sore, and shiny
Digestive discomfort, often with nausea and diarrhea
Feeling of pins, needles, and tingling in limbs
Hemolytic anemia
Excessive destruction of RBCs, or hemolysis leading to low erythorcyte count and low hemoglobin
Pathology of sickle cell
It occurs whenever oxygen levels are lowered. The altered hemoglobin is unstable and changes shape in hypoxemia. Sickle-cell shaped cells are too large to pass through the microcirculation and leads to multiple infarctions and areas of necrosis
Thalassemia
Genetic defect in which one or more genes for hemoglobin are missing or variant. This interferes with the production of globin chains, and the amount of hemoglobin synthesized and the number of RBCs is reduced
Two forms of thalassemia
Thalassemia Beta (autosomal dominant) and Thalassemia Alpha
Signs and Symptoms of Thalassemia
Child’s growth and development are impaired directly by the hypoxia and indirectly by fatigue and inactivity
Hyperactivity in the bone marrow leads to invasion of bone and impairs normal skeletal development
Heart failure develops as a result of the compensation mechanism increasing cardiac work load
Treatment for thalassemia
Blood transfusions
Iron chelation
Folate supplement
Pathology of hemophilia A
Deficit or abnormality of factor
X-linked recessive trait
Manifested in men, carried by women
S/S of hemophilia A
Prolonged bleeding after minor tissue trauma
Spontaneous bleeding into joints
Blood in feces
Diagnostic tests for hemophilia A
Bleeding time and PT normal
PTT, activated (PTT), coagulation time prolonged
Serum levels of factor VII are low
S/S of VonWillebrand Disease
Skin rashes Frequent nose bleeds Easy bruising Bleeding of gums Abnormal menstrual bleeding
Most common inherited clotting disorder
Hemophilia A
Most common hereditary clotting disorder
Von Willebrand
Disseminated Intravascular Coagulation
Involves both excessive bleeding and clotting
Excessive clotting in circulation
Clotting factors are reduced to a dangerous level and widespread uncontrollable hemorrhage results
Complications of disseminated intravascular coagulation
Obstetrical complications (abruptio placentae)
Infections
Carcinomas
Major trauma
Myelodisplastic syndrome
Diseases that involve inadequate production of cells by the bone marrow
Primary polycythemia (polycythemia vera)
Increased marrow production of erythrocytes and other cells in the bone marrow
Serum erythropoietin levels are low
Secondary polycythemia (erythrocytosis)
Increase in RBCs in response to prolonged hypoxia
Increased erythropoietin secretion
Compensation mechanism to provide increased oxygen support
Acute lympocytic leukemia (ALL)
Malignant cell - B lymphocytes
Age group - Young children
Acute myelogenous leukemia (AML)
Malignant cell - granulocytic stem cells
Age group - Adults
Chronic lymphocytic leukemia
Malignant cell - B lymphocytes
Age group - Adults greater than 50 degrees
Chronic myelogenous leukemia (CML)
Malignant cell - granulocytic stem cells
Age group - adults 3-50
Acute monocytic leukemia
Malignant cell - monocytes
Age group - adults
Hairy cell leukemia
Malignant cell - B lymphocytes
Age group - males greater than 50 years
Acute leukemias
High proportion of immature nonfucntional cells in bone marrow and peripheral circulation
Onset usually abrupt
Occurs in children and young adults
Chronic leukemias
Higher proportion of mature cells
Insidious onset
Common in older adults
Function of the lymphatic system
Returns excess interstitial fluid and protein to the blood
Filters and destroys unwanted material from body fluids
Initiates immune response (lymph nodes) by sensitizing B and T lymphocytes
Parts of lymphatic system
Lymphatic vessels (capillaries, branches, trunks, ducts, subclavian vein) Lympohid tissue (palantine and pharyngeal tonsils, spleen, and thymus gland)
Palatine and pharyngeal tonsils
Protection against bacterial infection in opening between nasal and oral cavities
First line of defense from external organisms
Functions of spleen
Defense
Hematopoiesis
RBC and platelet destruction
Reservoir for blood
Function of thymus gland
Final site of lymphocyte development before birth
Secretes hormones after birth to enable lymphocytes to develop into mature T cells
Vessels from R upper quadrant empty where
Into R lymphatic duct and returns lymph to general circulation via R subclavian vein
Most vessels in lymph system empty where
Into the thoracic duct in upper abdomen and thoracic cavity which drains into L subclavian vein
Multiple myeloma
Neoplastic disease of unknown etiology occurring in older adults involving the plasma cells (mature B lymphocytes)
Castleman Disease
Rare illness involving the overgrowth of lymphoid tissue
Parietal pericardium
Outer fibrous pericardium that anchors the heart to the diaphragm
Epicardium
Serous membrane that provides small amount of lubricating fluid within the pericardial cavity between the two pericardial membranes
Myocardium
Middle layer of the heart. Composed of specialized cardiac muscle cells that contract rhythmically and forcefully to pump blood throughout the organs.
Endocardium
Inner layer of the heart. Forms the four heart valves that separate the chambers of the heart and ensure one way flow of blood
Atrioventricular valves
R side (tricuspid) and L side (mitral or bicuspid)
Semilunar valves
aortic and pulmonary
Intercalated discs
Contain desmosomes which prevent muscle cells from separating during contraction
Gap junctions
Permit ions to pass from cell to cell to facilitate rapid transmission of impulses
SA Node
Usually initiates impulses (pacemaker of heart)
Location in wall of R atrium
Sinus Rhythm
Basic rate of impulses generated by SA node (70 bpm)
Can be altered by ANS fibers and circulating homrones
AV Node
Location in floor of R atrium
Only anatomical connection between the atrial and ventrical portions of the conduction system
P wave
Depolarization of atria
QRS wave
Depolarization of ventricles, Wave masks effect of atrial repolarization
T wave
Repolarization of ventricles (recovery phase)
Baroreceptors
Detect changes in BP, the cardiac center then responds through stimulation of SNS or PNS to alter rate/force of cardiac contractions
Located in aorta or internal carotid arteries
Sympathetic stimulation
Cardiac accelerator nerve
Increases HR (tachycardia) and contractility
Beta adrenergic receptors
Purpose of beta blockers
Block the increase in rate/force of contractions after heart has been damaged
Parasmypathetic stimulation
Vagus nerve Decreases HR (bradycardia)
Left anterior descending artery
Follows anterior interventricular sulcus downward over the surface of the heart. Supplies anterior wall of ventricles, anterior septum, and bundle branches
Left circumflex artery
Circles the exterior of the heart in L atrioventricular sulcus
Supplies L atrium and lateral/posterior walls of L ventricle
Right coronary artery
follows R AV sulcus on posterior surface of the heart. Supplies the R side of the heart and inferior portion of L ventricle and posterior interventricular septum. Also supplies SA and AV node
Diastole
Relaxation of myocardium required for filling chambers
Systole
Contraction of myocardium provides increase in pressure to eject blood
Lubb
Closure of AV valves at beginning of ventricular systole
Dubb
Closure of semilunar valves with ventricular diastole
Cardiac output
Blood ejected by a ventricle in 1 minute
Equation for cardiac output
CO=SVxHR
Stroke volume
volume of blood pumped out of 1 ventricle in 1 contraction
Preload
Mechanical state of heart at end of diastole with ventricles at their maximum volume
Afterload
Force required to ejected blood from ventricles. Determined by peripheral resistance to opening of the semilunar valves to arteries
Pulse pressure
difference between systolic & diastolic pressure
Peripheral resistance
Force opposing blood flow or amount of friction with the vessel walls encountered by the blood
Increases SNS output
Vasoconstriction and increased BP
Decreases SNS output
Vasodilation and decreased BP
Antidiuretic hormone
Increased BP
Aldosterone
Increased blood volume and blood pressure
Renin-angiotensin aldosterone
Vasoconstriction and increased BP
Low density lipoprotein
Transports chloesterol from liver to cells
High density lipoprotein
Transports cholesterol from cells to liver
Bradycardia
regular, but slow HR (less than 60 bpm)
Affected by vagal nerve or parasympathetic NS
Tachycardia
Regular rapid HR (100-160)
Normal response to sympathetic NS
Sick sinus syndrome
Marked by altering bradycardia and tachycardia
Premature atrial contractions or beat
Extra contraction (ectopic beats) Arise from a focus of irritable atrial muscle cells outside the conduction pathway (interfere with timing of next beat)
Atrial flutter
Atrial HR of 160 to 350 bpm
AV node delays conduction - ventricular rate slower
Atrial fibrillation
Rate over 350 BPM
Causes pooling of blood in atria
Thrombus formation is a risk
Heart blocks
Conduction excessively delayed or stopped at AV node of bundle of His
First degree block
Conduction delay between atrial and ventricular contractions (PR interval)
Second degree block
Every second to third atrial beat dropped at AV node
Longer delay leads to missed ventricular contraction
Third degree block
No transmission from atria to ventricles
Ventricles contract spontaneously at a slower rate (30-40 bpm) totally independent of atrial contraction
Bundle branch block
Interference with conduction in one of the bundle branches
Does not alter CO, but does show a wide QRS complex
Ventricular tachycardia
Reduce cardiac output as reduce diastole occurs
Ventricular fibrillation
Muscle fibers contract independently and rapidly
Cardiac standstill occurs if not treated immediately
Premature ventricular contractions
Additional beats from ventricular muscle or ectopic pacemaker
May lead to ventricullar fibrillation
L ventricle affected first (with CHF) when..
MI in L ventricle or essential HTN
R ventricle affected first (with CHF) when…
Pulmonary valve stenosis or pulmonary disease
Valvular defects
Interfere with normal flow of blood
Septal defects
Allow for mixing oxygenated blood with unoxygenated blood
L to R shunt
Blood from L side of heart recycled tot he right side and to the lungs
Results in increased blood volume in pulmonary circulation, a decreased CO, and inefficient system
R to L shunt
Unoxygenated blood from R side bypasses the lungs and enters the left side of the heart
Ventricular septal defect
Opening in the interventricular septum
Pressure usually higher in L therefore L to R shunt
Acyanotic condition unless respiratory condition increases pressure in R ventricle
Tetralogy of Fallot includes
Pulmonary valve stenosis
VSD
Detroposition of the aorta (to right over the VSD)
Right ventricular hypertrophy
Most common sites for PVD
Areas of bifurcation (abdominal aorta, carotid arteries, femoral and iliac arteries)
Thrombophlebitis
Development of a thrombus in an inflamed vein
Phlebothrombosis
Thrombus forms spontaneously without prior inflammation
