CHAPTER 11: THE CARDIOVASCULAR

SYSTEM--BLOOD

Transportation: of dissolved gases, nutrients, hormones, and metabolic wastes.

Regulation: of pH, blood clotting, body temperature and renal control.

Protection: against harmful toxins and pathogens

THE FUNCTIONS OF BLOOD

Blood volume: On average, 5-6 L in men and 4-5 L in women

Properties: Temperature: 38°C (100.4°F) Viscosity: high (5x more than

water) pH: 7.35-7.45 (slightly alkaline,

basic)Composition:

55% Plasma: matrix of blood that carries formed elements, gases, nutrients and wastes throughout the body. 92% Water 8% Electrolytes, Proteins & Nutrients

45% Formed Elements Red Blood Cells White Blood Cells Platelets

PROPERTIES & COMPOSITION OF BLOOD

Albumins (60%): of plasma proteins, produced in the liver, maintain osmotic balance (via water retention)

Globulins (35%): Immunoglobulins: attack foreign proteins and pathogens; antibodies

Transport (escort) Proteins: carry compounds that are not water soluble (i.e. lipids)

Fibrinogens: function in blood clotting when converted to fibrin.*Liver synthesizes many of these proteins.

PLASMA PROTEINS

GIVE BLOOD! SAVE LIVES!

Composition: (Hematocrit) 99.9 % Red Blood Cells

(Erythrocytes) <.1% White Blood Cells

(Leukocytes) ~ 1 to every 1000 RBCs

<.1% PlateletsHemopoiesis (hematopoiesis):

process of blood cell production Formed from embryonic blood

cells during 3 rd week of development

Formed in the liver and spleen during 2-5 th month of development

Formed in red bone marrow during adulthood

FORMED ELEMENTS

Shape: Biconcave discsMature RBCs lack

nuclei and other organs (Erythropoiesis)

Life cycle: ~120 days; 1% replaced each day (3 million new cells each second!)

Hemoglobin: made of two globular proteins; contains heme pigment which holds an iron ion that binds with oxygen

RED BLOOD CELLS (ERYTHROCYTES)

Cause: genetic mutation that affects the globular protein of hemoglobin

Sickled cells can easily clot and cause oxygen starvation of tissues

CLINICAL NOTE: SICKLE CELL ANEMIA

Four Blood Types: Type A: surface antigen A, plasma Anti-B Antibodies Type B: surface antigen B, plasma Anti-A Antibodies Type AB: surface antigen A & B, no anti-A or B antibodies Type O: no surface antigens A or B, plasma Anti-A & Anti-

B Antibodies (+/-): Determined by presence or absence of Rh antigens

on RBCsCross-reactions: mixing of blood types can cause

agglutination (clumping) of RBCs and eventual hemolysis (RBC destruction)

Anti-Rh antibodies are not normally present in plasma, unless exposure sensitizes an individual.

BLOOD TYPING (FIG. 11-7)

Hemolytic Disease of the Newborn Cause: mother and

child’s blood type differs and plasma antibodies from the mother cross the placenta and attack fetal RBCs

Usually occurs due to sensitization during delivery of previous child, which affects next pregnancy.

CLINICAL NOTE: HDN

Larger than RBCs, have nuclei, lack hemoglobin

Function: defense against pathogens, toxins, wastes and abnormal/damaged cells

Two groups: granulocytes & agranulocytes

Amoeboid movementMigration out of the

blood streamSome capable of

phagocytosis

WHITE BLOOD CELLS (LEUKOCYTES)

Granulocytes Neutrophils Eosinophils Basophils

Agranulocytes Monocytes Lymphocytes

WHITE BLOOD CELLS (LEUKOCYTES)FIG. 11-8 & TABLE 11-3

70% differential count

Active phagocytes (esp. bacteria)

Death recruits other WBCs and forms pus

Produced in bone marrow

NEUTROPHILS

2-4% differential count

Two-lobed and dyed red by eosin

Attack anti-body labeled materials by exocytosis (secretion) of toxins

Produced in bone marrow

EOSINOPHILS

<1% differential count

Deep purple/blue with many granules

Migrate to injury sites and stimulates inflammation and prevents blood clotting (heparin & histamine)

Produced in bone marrow

BASOPHILS

2-8% differential count

Large free or fixed macrophages

Aggressive phagocytes

Produced in bone marrow

MONOCYTES

20-30% differential count

Large nucleus with “halo” of cytoplasm

Integrates with lymphatic system

Do not rely on phagocytosis

Produced in bone marrow and lymphoid tissues

LYMPHOCYTES

Cell fragments that function in blood clotting

Formed from megakaryocytes

“Stick” together at injury sites to stop bleeding (hematosis)

PLATELETS (THROMBOCYTES)

Hemo “blood” + stasis “halt”: stops bleeding1. Vascular Phase: constriction of damaged blood vessels

(~30mins); blood vessel spasm2. Platelet Phase: “sticky” platelets form a platelet plug3. Coagulation Phase: conversion of fibrinogen to fibrin

HEMOSTASIS

Excessive coaguluation Thrombus: blood clot

attached to wall Embolus: moving blood

clot i.e. strokes, pulmonary

embolismInadequate coagulation

Hemophilia Missing clotting factor No cure, X-linked therefore

affects more males Symptoms including

excessive bleeding (external and internal)

CLINICAL NOTE: ABNORMAL HEMOSTASIS