Blood & Heart PP’s(6) A&P2

Cardiovascular System

pump (heart)

Conducting system (blood vessels)

Fluid medium (blood)

Type of connective tissue

Contains cells suspended in fluid matrix

Blood transports what?

To and from cells:

O2 + Co2

Nutrients

Hormones

Immune System Components

Waste products

O2, nutrients, Hormones (blood>IFluid>Cells)

Co2, Wastes (Cells>IFluid>blood)

Functions Blood

Transport dissolved subs

Regulate pH + Ions

Restriction of Fluid loss at injury sites

Defense against toxins + pathogens

Stabilization of body temp

Volume / Char of Blood

Blood V Liters 7% of BW kg

ADULT m 5-6L

ADULT f 4-5L

Gen Char of Blood

38c (100.4F) is norm TEMP

High Viscosity

Slight alkaline pH (7.35-7.45)

Whole Blood

Plasma

Fluid consisting of

Water

Dissolved Plasma Proteins

Other solutes

Formed Elements

Cells and Cell Fragments

3 Types Formed Elements

RBC/ erythrocytes

Most abundant 99.9% Elem

Transports respiratory gasses

WBC/ leukocytes

Part of immune system

Platelets

Cell frag involved in blood clotting

Hemopoiesis & Fractionation

Hemopoiesis

Process of prod formed elements

Done by myeloid and lymphoid stem cells in red bone marrow

Fractionation

Process of separating whole blood into plasma + formed elements

Hematocrit: % of whole blood V contrib by form elements

Males 46%, Females 42%

Plasma Comp

Makes 46-63% of blood V (abt half)

more than 90% water

Less than 10% solutes (most proteins)

Extra cell fluids include interstitial fluid and plasma

Plasma and IF have similar compositions

Materials diffuse across capillary walls

Water / Ions / Small solutes

Major difference between plasma and IF: PLASMA HAS PLASMA PROTEINS

Plasma Proteins

Majority 90>% are made by liver

High Concentration In blood (VS interstitial fluid)

LG size prevents protein from crossing capillary walls

Helps Maintain osmotic pressure

SPECIFIC proteins

Albumins 60% Trans molecules

Globulins 35% Antibodies / trans molecules

Fibrinogen 4% Forms clots

RBCs/ Erythrocytes

Makes up 99.9% bloods form elem

Red bc Hemoglobin

Pigment that gives whole blood its color

Protein that binds + trans respiratory gasses

Oxygen / Carbon Dioxide

Structure of RBCs

Small discs

Biconcave

Flexible plasma membrane

Contains hemoglobin (1/3 of weight)

NO NUCLEUS, lacks many organelles

Benefits of RBC shape

High surface- V ratio

Quick absorb + release oxygen

Discs form stacks (ROULEAUX)

Smooth flow through narrow blood vessels

Discs bend + flex entering small capillaries

7.8um RBC pass through 4um capillary

Life Span of RBCS

LACK nuclei, mitochondria, and ribosomes

X preform repairs so life span short (up 120 DAYS)

X make proteins so low energy demands

LACK mitochondria — RBC use anaerobic

Metabolism of glucose for energy

Ensures that all absorbed oxygen save for delivery to tissues

Hemoglobin Hb

Protein molecule trans respiratory gases

Each RBC has 280m Hb molecules

Each Hb molecule bind up to:

4 o2 molecules

4 co2 molecules

Hemoglobin Comp

Complex quaternary structure w/:

4 globular protein subunits

Each has one molecule of heme

Each heme contains one iron ion

Easily associates / dissociates w/ oxygen

(Oxyhemoglobin, deoxyhemoglobin)

Iron trans Oxygen

Subunits can bind to Co2

RBC Funct

Transport respiratory gasses

In LUNGS:

Release co2 and bind o2

Carries o2 from lungs > periphery = blood

In PERIPHERY:

Release oxygen to cells

Binds co2 and carries to lungs via BLOOD

RBC Form + Turnover

1% of circ RBCs wear our & replaced per day

when RBC wears, macrophages of liver, spleen, + bone marrow begin to recycle:

Monitor circ RBCs + engulf before membranes rupture (hemolyze)

Remove Hb molecules + iron from RBC that have ruptured (hemolyzed) in blood stream

Hemoglobin Conversion + Recycle

Macrophages break hemoglobin > components

Globular proteins (subunits) converted to amino acids (recycled)

Heme convert > biliverdin (green)

Biliverdin convert> bilirubin (yellow)

Bilirubin release > blood stream (waste)

Iron released > blood stream

Transferrin brings to red bone marrow

Used to make new Hgb (recycled)

Bilirubin

In blood stream is excreted by liver in bile

Convert > urobilins + stercobilins in LG intest

Elim in feces / urine

Pathophys: Jaundice

Yellow skin tone caused by bilirubin buildup assoc w/ immature / failing: LIVER

Hemoglobinuria / Hematuria

Hemoglobinuria: Hemoglobin breakdown products in urine due to excess hemolysis in blood stream

Hematuria: whole RBCs in urine due to kidney damage / UT tissue damage

Blood cell production

Erythropoiesis: RBC PRODUCTION

Occurs in red bone marrow

Hemocytoblasts (stem cells) divide to prod:

Myeloid stem cells become RBCs, platelets, all WBCs EXCEPT LYMPHOCYTES

Lymphoid stem cells become Lymphocytes

Stages of RBC Maturation

Myeloid stem cell

Proerythroblast (day 1)

Erythroblasts (3 stages; 2-4 days)

Reticulocyte (5-7 days)

Mature RBC

Regulation of Erythropoiesis

Building RBCs REQUIRES:

Amino Acids

Iron

Vitamins B12, B6, and Folic Acid

Erythropoietin (EPO) “Erythropoiesis stimulating hormone”

Hormone secrete by kidneys when o2 in peripheral tissues low (hypoxia)

Stims cell division in erythroblasts, increases Hb synthesis + RBC prod

Released during anemia, decreased blood flow > kidneys, oxygen from lungs, decrease (disease / high altitude)

Surface Antigens / Blood Types

Surface Antigens: glycoproteins on cell’s surface that ID cells to immune system:

Normal cells ignored and foreign cells attacked

Blood Types: genetically determined

By presence / absence of RBC surface antigens A,B,Rh

4 basic Blood Types

A surface antigen A

B surface antigen B

AB antigens A+B

O neither A/B

Antibodies and Antigens

Blood contains antibodies that attack all basic antigen types that are NOT present in Pt’s RBC

Type A: Type B antibodies

Type B: Type A antibodies

Type O: A+B antibodies

Type AB: neither A/B antibodies

Agglutinogens

Antigens on surface of RBCs that are screened by immune system

Plasma antibodies attack + agglutinate (clump) foreign antigens

Utilize agglutination to perform blood typing tests

Rh Factors

1st found in Rhesus monkey

Either Rh+ / Rh-

Rh+ means RBC have Rh surface antigen

(Blood will NEVER have Rh antibodies)

Rh- means RBC do not have Rh surface antigen

(Blood will ONLY have Rh antibodies after exposure to Rh antigen)

Hemolytic disease in pregnancy

Most Common form of disease Newborn develops after Rh- Woman carries Rh+ fetus

Mom not having Rh exposure now develops anti-Rh antibodies in response and crosses placenta to attack fetal RBCs

Cross Reactions in Transfusions

“Plasma antibody meets specific surface antigen”

Blood will agglutinate (clump) and hemolyze (RBC ruptures)

Occurs if Donor + Recipient blood types not compatible

Testing for Transfusion Compability

Performed on Donor + Recipient blood for compatibility

W/o cross-match, type O is universal donor

WBCs “leukocytes”

White - Does not have hemoglobin

Have nuclei + other organelles

Spherical

Life span: days - yrs

Most WBCs in connective tissue proper and lymphatic system organs

Small #’s in blood (5k-10k cells/ uL/ <1% bV)

WBC functs

Defend against pathogens

Remove toxins and wastes

Attack abnormal / damaged cells

4 Char of Circ WBCs

Can migrate out of bloodstream:

Margination: leaves cent bloodstream > out edges of blood vessel hugging endothelial walls

Emigration: Active process of WBCs squeezing through gaps in blood vessel walls to enter tissue space

Have amoeboid movement

Attracted to chemical stimuli (+ chemotaxis)

Some phagocytic (protect + engulf)

Neutrophils, Eosinophils, monocytes/ macrophages

5 types of WBCs

Neutrophils

Eosinophils

Basophils

Monocytes (become macrophages)

Lymphocytes

Neutrophils

Also called polymorphonuclear leukocytes

•50–70% of circulating WBCs (most abundant)

•Pale cytoplasm granules with:

•Lysosomal enzymes

•Bactericides (hydrogen peroxide and superoxide)

 

•Neutrophil Action

•Very active, first to attack bacteria

•Engulf and digest pathogens

•Release prostaglandins and leukotrienes

•Cause inflammation , Attract other cells

Lymphocytes

•20–30% of circulating WBCs (2nd most abundant)

•NO granules, Large round nucleus

•Migrate in and out of blood

•Mostly in connective tissues & lymphoid organs

•Are part of the body’s specific defense system

•There are 3 functional classes..

3 Funct classes of Lymphocytes

T cells

•Cell-mediated immunity

•Attack foreign cells directly

 

B cells

•Humoral immunity

•Differentiate into plasma cells

•Synthesize antibodies

2.Natural killer (NK) cells

•Detect and destroy abnormal tissue cells (cancers)

Monocytes

2–8% of circulating WBCs

•Are large with kidney bean shaped nucleus

•Enter peripheral tissues and become macrophages

•Aggressive phagocytes that engulf large particles and pathogens

•Secrete substances that attract immune system cells to injured area

Eosinophils (Acidophils)

2–4% of circulating WBCs

•Stain with red dye (called eosin), bilobed nucleus

•Attack large parasites

•Can phagocytize antibody marked bacteria

•Primarily excrete toxic compounds

•Nitric oxide

•Cytotoxic enzymes

•Are sensitive to allergens

•Control inflammation with enzymes that counteractinflammatory effects of neutrophils, basophils and mast cells

Basophils

Are less than 1% of circulating WBCs (relatively rare)

•Numerous blue stained granules

•Accumulate in damaged tissue where they release granules into interstitial fluid

•Histamine: Dilates blood vessels, inflammation

•Heparin: Prevents blood clotting

Differential Count + Change in WBC Profiles

Differential count gives the number of each type of WBC in a sample of 100 WBC

•Used to detect changes in WBC populations

•Gives information about the presence of infections, inflammation, and allergic reactions

WBC Disorders

Leukopenia

•Abnormally low WBC count

•Occurs during chemotherapy (RADIATION, HIV/AIDS)

Leukocytosis

•Abnormally high WBC count

•Indicates infection

Leukemia (CANCER OF BONE MARROW)

•Extremely high WBC count

WBC cell prod

ALL blood cell orig from Hemocytoblasts (prod myeloid stem cells + lymphoid stem cells)

Myeloid Stem Cells

Produce all WBCs Xlymphocytes

prod and mature in Red Bone marrow

Lymphoid Stem Cells

Prod Lympocytes (Lymphopoiesis - prod of lymphocytes)

Lymphocytes prod in red bone marrow but mature in lymphoid tissue

Reg of WBC prod

Colony-stimulating factors CSFs: Hormones that stimulate the prod of specific blood cells

MCSF stim monocyte prod

GCSF stim prod granulocytes (neutrophils, eosinophils, + basophils)

GMCSF stim granulocyte + monocyte prod

MultiCSF accelerates prod of granulocytes, monocytes, platelets, + RBCs

WBC Granulocytes

Neutrophils (bead / uneven nucleus)

Eosinophils (two lobe, red granules nucleus)

Basophils (nucleus usually not seen through dense blue granules) sponge like

WBC Agranulocytes

Monocytes (kidney / bean nucleus)

Lymphocytes (larger nucleus)

Platelets

Cell fragments: From LG cells called megakaryocytes

Has vesicles containing clotting factors, no nucleus

Circ for 9-12 days

Removed by phagocytes in spleen

2/3 in circ, 1/3 reserved for emergencies in Spleen

Platelet Counts

150K to 500K / umL

Thrombocytopenia:

Abnorm low platelet count

Major sign = bleeding (GI tract, under skin, mucous membranes)

Thrombocytosis

Abnorm high platelet count

Signals infection, inflammation, / cancer

3 Funct of Platelets

Release impt clotting chem

Temp plug damaged vessel walls

Contract to reduce size of break in vessel wall

Platelet Prod “Thromocytopoiesis”

Occurs in bone marrow

Hemocytoblasts > Myeloid stem cells > Megakaryocytes

Megakaryocytes:

Giant cells shed packets of cytoplasm that contain enzymes (ea packet is a platelet)

Hormones increasing platelet production

Thrombopoietin (TPO) increases platelet formation + megakaryocyte production

MultiCSF promotes formation + growth of megakaryocytes

Hemostasis

Cessation of Bleeding

Occurs in 3 phases

Vascular / Platelet / Coagulation

Vascular Phase of Hemostasis

A cut triggers vascular spasm

1.Endothelial cells contract and expose basement membrane to bloodstream

 

1. Endothelial cells

•Release chemical factors: ADP, tissue factor, and prostacyclin

•Release local hormones: endothelins

•Stimulate smooth muscle contraction and cell division

2. Endothelial plasma membranes become “sticky”

•Seal off broken end of vessel

Platelet Phase of Hemostasis

Platelet adhesion (attachment)

•To sticky endothelial cells

•To basement membranes

•To exposed collagen fibers

 

•Platelet aggregation (stick together)

•Forms platelet plug which closes small vessel breaks

 

•Activated platelets release chemicals that stimulate further aggregation (positive feedback!)

Coagulation Phase of Hemostasis

Blood clotting (coagulation):

• Blood changes from liquid to gel via a series of chemical reactions that culminate with the formation of fibrin

•Cascade reactions

•Chain reactions of clotting factors (Calcium, enzymes, and proenzymes)

•Form three pathways

•Convert circulating fibrinogen into insoluble fibrin

3 Hemostasis Coagulation Pathways

1.Extrinsic pathway

Begins outside of blood, damaged cells in vessel walls release tissue, factor TF3>leak into blood stream, TF3 + Ca +VII = enzyme complex> activates Factor X

2.Intrinsic pathway

Occurs slower, exposed collagen fibers activate pro enzymes in blood usually XII, Pathway assisted by platelet factor PF3, Series of reactions activates Factors V3 + IX which then activates Factor X

3.Common pathway

Intrinsic + extrinsic pathways converge, active X factor forms enzyme prothrombinase, converts prothrombin > enzyme thrombin> converts fibrinogen to fibrin> fibrin forms mesh trapping RBC, platelets to stop bleeding

Hemostasis Feedback Control

Thrombin Stimulates Blood Clotting by positive feedback

Stimulating formation of tissue factor,

Stimulating Release of PF3,

TF + PF3 lead to increased thrombin

Positive feedback loop: Accelerates clotting

Hemostasis FYI: Restriction of Blood Clotting

Plasma contains anticoagulants

•Antithrombin-III: inhibits clotting factors including thrombin

•Basophils and Mast cells release Heparin, a cofactor that increases activation of antithrombin-III

•Endothelial cells release thrombomodulin, which activates Protein C

•Protein C inactivates clotting factors & stimulates plasmin

•Prostacyclin inhibits platelet aggregation

Hemostasis Fibrinolysis

•Slow process of dissolving clot

•Thrombin and tissue plasminogen activator (t-PA)

•Activate plasminogen

•Plasminogen produces plasmin

•Digests fibrin strands to remove clot

Hemostasis Calcium Ions, Vitamin K, and Blood Clotting

Calcium ions (Ca2+) and vitamin K are both essential to the clotting process

•Deficiency leads to inability to clot

•Calcium utilized as a clotting factor

•Vitamin K is needed to produce 4 clotting factors

•Produced in large intestine, ingested in diet

•Warfarin: Anticoagulant medication that works by antagonizing Vitamin K