CHP 18 BLOOD

Hematology

the study of blood

myths about blood

-the “4 humors” keep in balance = heathy body

-drain “bad blood”

where were the first blood cells first seen?

in the 1st microscopes

circulatory vs cardiovascular system

CIRCULATORY = heart, blood vessels, AND BLOOD

CARDIOVASCULAR = heart and blood vessels ONLY

Functions of Circulatory System

-Transport

-Protection

-Regulation; homeostasis

What is blood?

Liquid connective tissue + cells + extracellular matrix

What are the two main components of blood

1) Blood Plasma = liquid portion = matrix

2) Formed Elements = solid stuff = blood cells/fragments (SEVEN OF THEM)

What are the 7 kinds of formed elements in blood?

1) Erythrocytes = RBCs

2) Thrombocytes = platelets (cell fragments from bone marrow)

3) Leukocytes = WBCs

• Granulocytes

  • Neutrophils

  • Eosinophils

  • Basophils

• Agranulocytes

  • lymphocytes

  • monocytes

How to remember most common to least common leukocytes

NEVER

LET

MONKEYS

EAT

BANANAS

What is a hematocrit

centrifuge blood to separate components (how much plasma compared to blood cells?)

therefore how much oxygen blood can carry

levels of hematocrit in the bottle:

HEAVIEST to LIGHTEST

-Erythrocytes (RBCs)

-Leukocytes (WBCs) + platelets (*BUFFY COAT*)

-Plasma

The main categories of STUFF in plasma

-Plasma Proteins (Albumins, Globulins, Fibrinogen)

-Nitrogenous compounds (free amino acids or nitrogenous wastes from catabolism)

-nutrients

-gases (O2 + CO2 + nitrogen)

-electrolytes (Na+)

what are the plasma proteins?

1) Albumins = smallest most abundant, viscosity, flow, osmolarity

2) Globulins (antibodies) = immune functions

• alpha

• Beta

• Gamma

3) Fibrinogen (PRE PROTEIN) = precursor of fibrin (that will help form blood clots)

how are plasma proteins made

albumins and fibrinogen by the LIVER

globulins by plasma cells

What is Viscosity?

“how thick is the fluid?”

-resistance to flow

-plasma + whole blood is more viscous than water (IMPORTANT FOR CIRCULATORY FUNCTION)

Osmolarity of Blood

the total molarity of dissolved particles that cannot pass through blood vessel wall

ex: NaCl (2 osmolar)

ex: MgCl2 (3 osmolar)

levels of osmolarity and impacts

TOO HIGH = BLOOD absorbs TOO MUCH WATER, blood pressure increases

TOO LOW = TOO MUCH WATER in TISSUE, blood pressure drops = edema

PERFECT= body regulating sodium ions, proteins, red blood cells effectively

Hemopoiesis

(Hemogenesis)

production of blood

where does hemopoiesis occur

-Hemopoietic tissues (AKA preembryonic/fetus tissues)

-hemocytoblasts

Hemopoiesis in Hemopoietic tissues

1) Yolk Sac = stem cells turn into red blood cells

2) liver = stops making RBCs at birth

3) Spleen = remains involved w lymphocyte (one of the 7 formed elements) production

hemopoiesis in red bone marrow

*MAKES ALL 7 FORMED ELEMENTS

a) Mulipotent stem cells (many kinds) called HEMOCYTOBLASTS (cells that build blood)

b) Colony-forming unit = specialized, forms only one class of formed elements

Myeloid Hemopoiesis

Blood formation in the bone marrow

Lymphoid Hemopoiesis

Blood formation in the lymphatic organs (beyond infancy only includes lymphocytes)

the main function of Erythrocytes

THE PIZZA DELIVERY GUY

GAS TRANSPORT

• carry oxygen FROM lungs to cell tissues

• carry CO2 from cells TO lungs

why are erythrocytes shaped the way they are

-biconcave shape (lost nearly all organelles during development)

-we don’t want to loose oxygen (cause they are the main gas transport guys);

• Anaerobic fermentation to make ATP (no oxygen use)

• no nucleus + DNA (no protein synthesis or mitosis bc that uses high amounts of ATP)

How do blood cells keep their shape?

cytoskeletal proteins (spectrin and actin) give membrane durability and reliance so the blood cells can squeeze through small capillaries

TWO IMPORTANT guys that assist in gas transport in blood cells

Hemoglobin = deliver oxygen to tissues and CO2 to the lungs

Carbonic anhydrase (in the cytoplasm) = takes CO2 and makes carbonic acid = NO BUBBLES

Hemoglobin contains:

FOUR PROTEIN CHAINS

-adult = 2 beta + 2 alpha

-fetus = 2 gamma + 2 alpha

FOUR HEME GROUPS

-bind to Fe (iron) in the middle

-what oxygen clings to giving the red color to blood

Why hematocrit levels lower in women?

-men have more ANDROGENS (testosterone) that stimulate RBC cycle

-menstrual losses

-higher % of body fat (cause less androgens in women)

Erythropoiesis (PROCESS!!!!)

A Type of hemopoiesis specially for red blood cells

1)hemopoietic stem cell

2) erythrocyte colony forming unit (stimulated by erythropoietin = MAKE BLASTS)

3)erythroblast

4) shrinks + looses nucleus = reticulocyte (immature cell)

5) erythrocyte

Process of Liver Metabolism (PROCESS!!!)

1) EAT IRON

2)stomach acid takes Fe3 to Fe2

3)Fe2 binds to gastroferritin

4)transport to small intestine (highly acidic to mildly basic = RELEASE IRON)

5) iron binds again to transferrin

6) goes to liver

7) binds to apoferritin to be stored as ferritin OR remaining transferrin keeps going past liver to make hemoglobin, myoglobin, etc

How and why do we store iron?

iron = allows us to store oxygen in our cells and not have bacterial growth

Liver apoferritin binds to make ferritin (YAY WE CAN STORE IRON!)

Erythrocyte Homeostasis (PROCESS!!!)

TO MAKE OR DONT MAKE BLOOD CELLS (negative feedback loop)

1) DROP in RBCs = hypoxemia detected by kidneys

2)produces erythropoietin

3)release it

4) stimulates growth of red bone marrow

5) increases erythropoiesis= more RBCs= more O2= happy body

why might we increase erythropoiesis?

-hypoxemia (low levels of O2)

-high altitude

-increase in exercise

-loss of lung tissue in emphysema

Erythrocyte Death (PROCESS!!!)

- circulate for 120 days until death starts

1) IN THE SPLEEN AND LIVER, separate Heme from Globin

2) Globin into amino acids, iron removed from heme

3) Heme into biliverdin (green)

4) converted into bilirubin (yellow)

• either out as urine

• or continues to liver

5) remove bilirubin into bile

6) into small intestine to make urobilinogen (brown) = feces

Polycythemia

having an excessive amount of RBCs

-DANGERS; increase in blood volume, pressure, viscosity (clotting) = stroke, heart failure, embolism

Primary Polycythemia

BAD

cancer of erythropoietic cell line In red bone marrow

too high RBC= too viscous= too hard on the heart

Secondary Polycythemia

Eh its not too horrible

from dehydration, high altitude, physical conditioning, emphysema

Anemia

low RBC concentration

3 consequences:

1) tissue hypoxia and necrosis (low oxygen and death)

2) tissue edema (too much water weight)

3) blood viscosity low (cardiac failure)

3 causes of Anemia

1) Inadequate erthropoeisis (We don’t make enough)

• Iron-Deficiency anemia

• pernicious anemia (autoimmune attack on stomach = not enough B12)

• hypoplastic anemia (slowing of erythropoiesis)

• aplastic anemia (complete STOP of erythropoiesis)

2) Hemorrhagic anemias (we loose too many, bleeding)

3) Hemolytic anemias (we destroy too many)

Blood Antigens (Agglutinogens)

-sit on cell surface of blood cells

-determine blood type

-over 200 known, 3 specific (A,B,Rh)

Blood Antibodies (Agglutinins)

-proteins secreted by plasma cells to bind to antigens and MARK them for destruction

-found in plasma

Agglutination

“clumping”

antibody binded to antigen

= incompatible transfusion = BAD

What determines RBC antigens

glycolipids on RBC surface

Universal donor and receive is:

donor = O-

receiver = AB+

Hemolytic disease of the newborn

Rogam given to mom to give her antibodies to neutralize Rh factor

so even if the second pregnancy is Rh+, baby won’t be attacked by moms antibodies

Leukocytes functions

-least abundant formed element

-protect against pathogens and microorganisms

-roam around mostly and do not stay in the bloodstream

-have organells for protein synthesis

-ALL have lysosomes (nonspecific granules)
-granulocytes or agranulocytes

Neutrophils

-granulocyte leukocyte

-msot common

-antibacterial

think "pus”

Eosinophils

-granulocyte leukocyte

-parasitic infections, destroy large

Basophils

-granulocyte leukocyte

-”allergies”

-histamine = increases blood flow to injured area

-heparin = anticlogging, let more WBCs into the area

Lymphocytes

agranulocyte leukocyte

-most complicated

-destory human cells

-coordinate actions of other immune cells

-’the big guy’

monocytes

agranulocyte leukocyte

transform into macrophages

“sprinkle” cells with antibodies to dsestory them

Leukopoiesis

type of hemopoiesis specific to production of white blood cells

hemopoietic stem cells turn into:

1) myeoblasts = granulocytes (in bone red bone marrow)

2) monoblasts = monocytes (in red bone marrow)

3) lymphoblasts = lymphocytes

Thrombocytes

-platelets

-fragments of megakaryocytes

-HUGE can be seen w naked eye

Functions of thrombocytes

• vasoconstrictors (smaller pipes)

• Stick together (plugs)

• Secrete clotting factors (so fibrin can make clots)

• attract neutrophils and monocytes to inflammation sites to phagocytize bacteria

• secrete growth factors (HEAL)

Thrombopoiesis

type of hemopoiesis specific to making thrombocytes

stem cells to megakaryoblasts to megakaryocytes

Hemostasis (PROCESS!!!)

STOPPING bleeding

1) vascular spasm

• pain sensed = constrict the blood vessel

• platelets release serotonin = “time to repair”

2) platelet plug formation

• broken vessels expose collagen

• STICKYYYY makes the platelets stick together = plug

• releasing of a lot of stuff as the platelets stick together

• Positive feedback loop continues until the vessel is sealed

3) blood clotting (coagulation)

• converting plasma protein (fibrinogen) into fibrin to make framework of CLOT

• procoagulants (clotting factors) activate a reaction cascade

• IF AN EXTERNAL CONFLICT = extrinsic pathway = two proteins = fast

• IF INTERNAL CONFLICT = intrinsic pathway = four proteins = complicated

• BOTH CONVERGE on common pathway at Factor X, AND BOTH NEED CALCIUM

• then it goes to Factor V (take prothrombin and convert to thrombin)

• makes fibrinogen

• convert to fibrin

• make a fibrin polymer

• BLOOD CLOT HORRAY

hemorrhage

excessive bleeding

Fibrinolysis

dissolution of a clot

-Factor XII speeds up kallikrein enzyme that converts plasminogen into plasmin (BREAKS UP THE CLOT)

how to prevent random clotting

1) Platelet repulsion (non stickiness)

2) Thrombin Dilution (blood flows rapidly)

3) natural anticoagulants

• Heparin = interferes with prothrombin activator

• Antithrombin = deactivates thrombin

hemophilia (3 types)

hereditary diseases w messed up factors

1) SEX LINKED (recessive X chromosome)

• Hemophilia A = missing factor IX, bleed out easily

• Hemophilia B = missing factor IX

2) AUTOSOMAL

• Hemophilia C = missing factor XI

hematoma

masses of clotted blood in the tissues (bruises)

Thrombosis

abnormal clotting in UNBROKEN vessels

thrombus

stationary clot

embolus

clot that moves around

Pulmonary embolism

clot breaks free, travels from veins to lungs

Infarction

tissues death that can occur is clot blocks blood supply to an organ

How to prevent clots

1) Have less Vitamin K in your diet (because Vitamin K is required for formation of clotting factors)

2)Aspirin = suppresses thromboxane A2

3) anticoagulants: medical leeches snake venom

how to get rid of clots clinically?

1) Dissolving clots that have already formed

• Streptokinase = enzyme made by streptococci bacteria

• Tissue Plasminogen activator (TPA) = faster, more specific, transgenic bacteria

• Hementin = produced by giant amazon leech