Lecture Exam 2 Flashcards
Non-living fluid matrix of blood.
Plasma
3 Formed Elements of Blood
Platelets, Erythrocytes, Leukocytes
Red Blood Cells are Called:
Erythrocytes
White Blood Cells are called:
Leukocytes
3 Layers of Blood when spun in a centrifuge
Plasma, Buffy Coat (WBC/Platelets), Erythrocytes
Plasma should make up how much of a hematocrit?
55%
Erythrocytes should make up how much of a hematocrit?
45%
How do you figure out how much of an element in a hematocrit?
Column of element/column of whole tube multiplied by 100
Function of Leukocytes
Protect body from bacteria, viruses, parasites, toxins, and tumor cells.
Diapedisis
The way that WBC’s leave the capillaries towards infection using ameboid motion and positive chemotaxis
Leukocytosis
Increased production of WBC’s, normal response to infection.
3 Granulocytes
Neutrophils, Eosinophils, Basophils
2 Agranulocytes
Lymphocytes, Monocytes
Most common Leukocytes to Least Common
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
Characteristics of Granulocytes
Cytoplasmic granules, shorter lived that RBC’s, Lobed nuclei, all phagocytic.
Characteristics of Neutrophils
Most abundant, 3-6 lobes in nucleus, Larger than RBC’s, contain defensins, phagocytize bacteria
Characteristics of Eosinophils
Bi-lobed nucleus, Red granules, Larger than RBC’s, Defend against parasitic worms, Role in allergies and asthma
Characteristics of Basophils
Deep Purple nucleus, Larger than RBC’s, Least abundant, contain histamine
Histamine
Inflammatory chemical that dilates blood vessels to attract WBC’s to site of infection.
Characteristics of Lymphocytes
Deep purple, circular nuclei, Mostly in lymphoid tissue, Mount immune response
Characteristics of Monocytes
Kidney shaped nuclei, very large.
Function of Monocytes
Differentiate into microphages and enter tissues, actively phagocytic, activate lymphocytes to mount immune response.
Leukopoiesis
Production of WBC’s.
Leukopoiesis is stimulated by:
Interleukins and Colony Stimulating Factors
All leukocytes originate from:
Hemocytoblasts
Where are the chemical messengers found that stimulate Leukopoiesis?
Red Bone Marrow and Mature WBC’s
Leukopenia
Abnormally low WBC count.
What causes Leukopenia?
Glucocorticoids or anti-cancer drugs
What is Leukemia?
The Cancerous overproduction of abnormal WBC’s. Fill red bone marrow .
Myeloid Leukemia
Myoblast decendents (granulocytes)
Lymphocytic Leukemia
Involves lymphocytes
Acute Leukemia
Derives from Stem Cells
Chronic Leukemia
Derives from later cell stages.
Infectious Mononucleosis
Excessive numbers of atypical a granulocytes. Caused by Epstein Barr Virus
Symptoms of Infectious Mononucleosis
Tired, achy, sore throat, low fever
How do you treat infectious mononucleosis
Runs course with rest
Sickle Cell Anemia
Red Blood Cells are sickle shaped, not round. Rupture easily and block small vessels.
Pernicious Anemia
Large and Odd Shaped RBC’s
Whole Blood Transfusions
Used when blood loss is rapid and substantial (>30%).
Packed Red Cell Transfusions
Transfused in other cases, restore Oxygen carrying capacity.
Loss of ______ or more blood can be fatal.
30%
Transfusions of incompatible blood can be _________.
Fatal
Antigens (Agglutinogens)
Generate Immune Response
Antibodies (Agglutinins)
Pre-formed Anti-A or Anti-B antibodies
Type A blood would have:
Antigens: A Antibodies: Anti-B
Type B blood would have:
Antigens: B Antibodies: Anti-A
Type AB blood would have:
Antigens: A and B Antibodies: None
Type O blood would have:
Antigens: None Antibodies: Anti-A and Anti-B
Which type of blood is a universal donor?
Type O
Which type of blood is a universal receiver?
Type AB
Agglutinated
Clumped together
If someone’s blood type is O negative, what antigen are they missing?
RH antigen
How many times does someone who is RH- have to be transfused with RH+ blood to get a reaction.
The second time there is a reaction.
Someone will only produce RH antibodies if:
A mom is carrying an RH+ baby, and individual who is RH- receives RH+ blood.
Erythroblastosis Fetalis
When an RH- mom is carrying an RH+ baby, the second time the baby may become anemic or hypoxic.
RhoGRAM Serum
Contains artificial RH antibodies so that the mother of a baby doesn’t produce RH antibodies and attacks the fetus.
Results of Transfusion Reactions
Diminished O carrying capacity, Diminished blood flow beyond blocked vessels, Ruptured cells release hemoglobin and cause kidney failure.
Treatment for transfusion reactions
Fluids and diuretics to wash out hemoglobin.
Low Blood Volume can cause_____ and_____.
Shock and Death
3 Functions of Blood:
Distribution, Regulation, Protection
Blood Distribution:
Distributes O, Nutrients, Hormones. Removes metabolic waste.
Blood Regulation:
Maintains body temperature, pH, Fluid volume
Lower blood pH than normal:
Acidosis
Higher blood pH than normal:
Alkalosis
Blood Protection:
Provides Leukocytes
Plasma
Non-living fluid matrix of blood
Blood Plasma Characteristics
90% Water, Least heavy layer and the most abundant, Solutes
Solutes of Blood Plasma
Electrolytes and Plasma Proteins (albumin)
Albumin
Regulates osmotic pressure
Function of Erythrocytes
Respiratory gas transport
Hemoglobin
Binds reversibly with Oxygen
Characteristics of Erythrocytes
Small, biconcave, high hemoglobin content, no mitochondria, aneucleate
Globin
Composed of 4 polypeptide chains
Heme
Pigment bonded to each globin chain. Iron atom binds with 1 Oxygen atom.
How many O atoms can each Hb (Hemoglobin) molecule bind to?
4
Oxyhemoglobin
Produced by O2 loading into lungs. Ruby red in color.
Deoxyhemoglobin
Produced by O2 unloading in tissues. Dark red in color.
Carbaminohemoglobin
Produced when CO2 loads in tissues. 20% of CO2 in blood binds to Hb.
Hematopoiesis
Production of blood cells
Blood cell formation occurs where?
Red bone marrow
Erythropoesis
Production of Red Blood Cells
All blood cells arise from a ____________.
Hemocytoblast
Hormones and growth factors influence ___________ to turn into erythrocytes.
Myeloid Stem Cells
Balance of RBC production and destruction depends on:
Hormonal Controls and Dietary requirements
Too few RBC’s leads to_______
Tissue Hypoxia
Too many RBC’s leads to ________
Blood viscosity
Erythropoietin (EPO)
Glycoprotein hormone in kidneys that stimulates RBC production.
EPO production is increased by ______.
Hypoxia
EPO is increased by hypoxia due to:
Decreased RBC’s, Insufficient Hemoglobin, Reduced O availability
Dietary Requirements for Erythropoesis
Nutrients and structural materials, Iron, B complex vitamins
What element is necessary for hemoglobin synthesis?
Iron
What type of vitamins are necessary for DNA synthesis?
B complex vitamins (Folic, B12)
How long does an RBC live in the bloodstream?
About 100 days
What happens to the parts of RBC’s that cannot be reused?
Excrete them
What part of the RBC must be reused?
Hemoglobin
When an RBC is destroyed Heme is taken where?
Fe goes back to the blood stream, the rest is taken to the liver.
When an RBC is destroyed Globin is taken where?
It is turned into amino acids
Anemia
Bloods Oxygen carrying capacity is too low to support normal metabolism
Polycythemia
Abnormal excess of erythrocytes
Symptoms of Anemia
Fatigue, pallor, shortness of breath, chills
Causes of Anemia
Blood loss, Low RBC production, High RBC destruction
Acute Hemmorhagic Anemia
Rapid loss of blood quickly
Chronic Hemmorhagic Anemia
Slight, but persistent blood loss
Iron deficiency anemia
Caused by hemmorhagic anemia, low iron intake or impaired absorption
Pernicious Anemia Causes
Autoimmune Disease, Lack of ability to absorb B12 to have cell division.
Renal Anemia
Lack of Erythropoeitin
Aplastic Anemia
Destruction or inhibition of red bone marrow by chemicals, drugs, radiation or viruses
Hemolytic Anemias
Premature RBC lysis
Thalassemias
Where one globin chain is absent or faulty
Sickle Cell Anemia occurs mostly in what race of people?
Black/African
You have a better chance of surviving malaria if you have how many copies of the sickle cell gene?
One
If you have one copy of the sickle cell gene you have ________ if you have two copies you have ________.
Sickle Cell Trait, Sickle Cell Anemia
Polycythemia Vera
Bone Marrow Cancer
Secondary Polycythemia
Less O2 available (high altitude) or EPO production increases.
Blood Doping
Artificially induced polycythemia to increase O2 carrying capacity. Used by athletes.
Function of Platelets
Clotting Process, Form temporary plug to help seal breaks in vessel walls.
Why is blood doping dangerous?
Blood can become too viscous
Platelets are made from:
Ruptured cytoplasmic elements of a megakarocyte.
What hormone regulates the formation of platelets?
Thrombopoieten
Hemostasis
3 reactions that help prevent the loss of blood from breaks in the vessel walls.
Hemostasis is _______, ________, and _________
Fast, localized, and highly controlled
What coordinates Hemostasis?
Clotting Factors
3 Steps to Hemostasis
Vascular Spasm, Platelet Plug Formation, Coagulation of Blood
Vascular Spasm
Damaged blood vessel responds to injury by constricting.
Vasoconstriction
The constriction of a blood vessel
Triggers of a Vascular Spasm
Direct injury to blood vessel wall, Chemicals released by endothelial cells and platelets, Local pain receptor reflexes
von Willebrand Factor
Plasma protein that helps platelets stick to collagen fibers.
Damage to blood vessel exposes ___________
Collagen fibers
Platelets release _________ to make nearby platelets to become spiked and sticky.
Chemical messengers
Chemical Messengers that cause platelets to become sticky
Adenosinediphosphate (ADP), Serotonin, Thromboxane A2
In coagulation, platelet plug is reinforced with _________.
Fibrin Threads
In coagulation blood is formed from ______ to _______.
Liquid to gel
3 phases of coagulation:
Prothrombin activator formed, Prothrombin turns into thrombin, Thrombin catalyzes fibrinogen to fibrin
Factor __ works to form the prothrombin activator
X
Coagulation phase 1
Factor X works to form prothrombin activator
Coagulation phase 2
Prothrombin activator catalyzes transformation of prothrombin to thrombin
Coagulation phase 3
Thrombin catalyzes the transformation of fibrinogen to fibrin.
Fibrinogen is _________ while fibrin is ________
soluble, insoluble
Thrombin also activates factor _________ or __________.
Factor XIII, Fibrin stabilizing factor
Clot retraction
Platelets contract, drawing edges of ruptured blood vessels together.
Vessel Healing
Stimulates cells of vessel walls to divide
Platelets release __________ for vessel healing
Platelet Derived Growth Factor (PDGF)
Endothelial cells release ________ for vessel healing
Vascular Endothelial Growth Factor (VEGF)
Fibrinolysis
Removes unneeded clots after healing
Plasmin
Fibrin-digesting enzyme
Homeostatic Mechanisms limiting clot growth
Removal of clotting factors, Inhibition of activated clotting factors
Antithrombin III
Inactivates thrombin
Heparin
Enhances Antithrombin III
Thromboembolic Disorders
Undesirable clot formation
Bleeding Disorders
Unable to clot
Disseminated Intravascular Coagulation (DIC)
Clotting and Bleeding issues
Thrombus
Stationary clot that develops and persists in an unbroken vessel
Thrombosis
Formation of a blood clot inside a vessel that blocks the flow of blood.
Embolus
A Thrombus that is freely floating throughout the body
Embolism
Stuck clot
4 Anticoagulant Drugs
Aspirin, Heparin, Warfarin, Dabigitran
Aspirin
Inhibits Thromboxane A2
Warfarin (Coumadin)
Interferes with Vitamin K production of clotting factors
Dabigitran
Inhibits thrombin
2 Causes of Deficient Clotting
Circulating platelet deficiency, Deficiency of clotting factors
Thrombocytopenia
Platelet Deficiency
Circulating platelet deficiency can come from ________
Red bone marrow destruction
Deficiency of Clotting factors can come from________
Impaired liver function, Vitamin K deficiency, Hepititis or Cirrohsis
Hemophilia
A genetic disease, Factor VIII, Minor tissue trauma causes prolonged bleeding
Hemophilia ____ is the most common type
A
Disseminated Intravascular Coagulation (DIC)
Clotting in intact blood vessels, severe bleeding because residual blood unable to clot.
DIC can happen because of
Pregnancy issues, Septicemia, Incompatible Blood Transfusions
Coordinated Heartbeat is a function of _____ and _____
Gap junctions, Intrinsic conduction system
Cardiac Pacemaker Cells
Noncontractile cells with unstable resting membrane potential
Cardiac Pacemaker Cells do two things:
Drift toward depolarization, Trigger rhythmic contractions through action potentials
3 parts of Action Potential
Pacemaker Potential, Depolarization, Repolarization
Electrical Impulse of the Heart Passes in this order:
SA node, AV note, Bundles of His, Purkinje Fibers (Subendocardial Conducting Network)
Sino Atrial Node
Drives Heart Rate, Generates the impulse.
Atrioventricular Node
Impulse Pauses here
Atrioventricular Bundle
Connects Atria to the Ventricles
Bundle Branches
Conduct impulses through the inter ventricular septum
Subendocardial Conducting Network
Depolarizes contractile cells of both ventricles
SA node has ______ bpm
75
AV node has ______ bpm
50
AV bundle and Purkinje Fibers have _____ bpm
30
Arrythmias
Irregular Heart Rhythms
Fibrillation
Rapid, irregular contractions
Defibrillation
Resetting the electrical activity of the heart
Homeostatic Imbalances of the Electrical System of the Heart
Arrhythmias, Fibrillation, Uncoordinated atrial and ventricular contractions
Ectopic Focus
Abnormal pacemaker caused by defects with SA node. AV node sets a junctional rhythm (45-60bpm)
Extrasystole
Premature contraction. Can be caused by nicotine or caffeine
Heart Block
Few or no impulses reach ventricles because of defective AV node. Too slow for life, need artificial pacemaker to treat.
Extrinsic Innervation of the Heart:
Heartbeat modified by ANS via cardiac centers in the brainstem.
Cardioacceleratory Center
Sympathetic, accelerates via AV, SA nodes, heart muscle and coronary arteries.