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Circulatory system functions

Transport of material via blood

1. Respiration
Lungs —o2—>tissues
Tissues —co2 -> lungs

2. Nutrition
GI Tract —-> tissues

3. Excretion
Tissues —waste—> kidneys

4. Regulation
a. pH
b. temp.
- dermal vasoconstriction/vasodilation
- distribution of heat around the body
c. fluid volume balance
d. hormones

5. Protection
a. infection - white blood cells
b. hemostasis


Red and blue

Red = high o2, low co2

Blue = low o2, high co2


Closed circulatory system

A system in which the blood is always confined within blood vessels and the blood + tissues never mix


Basic circulatory outlay (systemic circulation) * pic in notes

* use pic


Lymph nodes

All lymph must pass through lymph nodes before being dumped into venous blood

Lymph node - like a “filter”

- composed of reticular CT on which
defensive body cells are hung

Defensive body cells:



Both: look for bad stuff in the lymph
(lymph- stuff that comes from the


Body defenses

1st line:
innate defenses
-> deny entrance and limit spread of microorganisms

Physical barriers:
a. skin
- most microbes can’t pass unbroken
b. mucus membranes
- basement membranes - hard to pass
c. mucociliary Action
- in respiratory tract

Chemical barriers:
- stomach acid -> kills microbes
- sweat
- tears
- sebum
All: contain bacteria killing proteins
* skin pH is acidic - “acid mantle”

Biological barriers:
non specific white blood cells
- neutrophils
-> 1st responders, 1st on scene when an
infection takes hold
- macrophages
-> (monocytes), stand guard in tissues-
eat bad stuff

(Non specific lymphocyte):
Natural killer cells
-> cause lysis of abnormal body cells


Non specific defenses continued

Circulating chemicals
1. Complement system (proteins)
- assists in antibody attack of non self cells
- attract white blood cells
- increase local inflammation

2. Interferons
- inhibit viral replication
- attract white blood cells



Body’s response to tissue damage

- red
- raised (swollen -> edema)
- elevated temp
- pain


Inflammation process

Damaged tissue cells
— release —>
- proteins
- prostaglandins
- other stuff
All: activate local *mast cells*

Mast cells:
- central players in inflammation
- secrete:
- heparin
- prostaglandins
- other stuff
- histamine
- serotonin
All: inflammation


An inflammation reaction
* pic in notes

Mast cells -> pivotal in inflammation

Damaged tissue

- attracts phagocytes (especially neutrophils)

Neutrophils secrete compounds:
- attract more phagocytes
- stimulate CT repair
- eat bad stuff

- compliment proteins leak into damaged tissue from blood

- clotting factors: clot
-> encapsulates the area
- called “walling off”


Immune system

Prevent infection

Normal life time ->
exposed to 10,000 - 20,000 immunogens

Immunogen -> something that can stimulate the immune system
- bacteria
- viruses
- fungi
- uni/multicellular parasites
^^^ - pathogens - can cause disease
- allergens
- produce a superfluous response
- immune response causes symptoms


Immunogens —> produces antigens

-> biomolecules (usually proteins like glycoproteins) that can simulate an immune response because they are detected by the immune system as being “non self” - foreign



Specific / past exposure to specific antigen

Based directly on the activity of lymphocytes


Types of immunity (humoral)

Humoral immunity
-> based upon the activity of B Lymphocytes (B cells)

Foreign antigen

-detected by->

B cell


Many B cells (plasma cells)


Antibodies (soluble protein molecules)




Types of immunity (cell mediated activity)

Cell Mediate Activity
-> T cells

Your own abnormal body cells
- faulty surface markers

-detected by->

T cell

-proliferate into->

Helper T cells
-> coordinate immune attack


Killer T cells
-> directly attack and destroy your
abnormal body cells


Humoral immune response

*clonal selection*

- you have millions of different strains of B cells in your body
-> these strains differ in the shape of their
*surface protein receptors*
ex. Specific B cell will have a receptor that fits specific antigen


1. Receptor binds with the antigen and stimulates rapid mitosis
-> produces millions of “clones” of that
-> most of those clones differentiate into
plasma cells
-> some form memory cells which hang out
and wait for reinfection

2. Plasma cells have rough endoplasmic reticulum and secrete antibodies
-> antibodies have antibody active sites that
match the same sharp as the original
B cell receptor and therefore can stick to
foreign antigen

* see graph in notes comparing response with memory cells and primary response


Cell mediated immunity - T cells

a. Killer T cell response

Killer T cells (Tk) = CD8 cells (cytotoxic T cells)

Background (Tk):
- all your body cells have glycoprotein surface markers called MHC 1 Markers

MHC 1 Markers
-> identify the cell as “self”

A.) Killer T response:

1. Cell infected by virus

2. Golgi from virus infected cell produces MCHI/Antigen (“secret flag”)

3. Tk strain fits receptor or infected cell, then undergoes clonal selection
-> produce millions of that variety of killer
T cell clones that are active
-> a few become memory cells

B.) Helper T response
- require the participation of macrophages/monocytes

- macrophages/monocytes have glycoprotein surface markers called MHC 2 Markers

MHC 2 Markers:
- found only on macrophages, monocytes, and lymphocytes


1. Macrophage engulfs antigen, becomes “antigen presenting cell”

2. Within macrophage, antigen is chopped into pieces -> “antigen processing”
-> fragments are sent into Golgi which
produces MCH 2 Marker on macrophage

3. Macrophage detected by T helper strain, fits on to macrophage receptor -> “antigen presentation”, and then undergoes clonal selection
-> most become T helper clones
-> a few become memory cells


Effect of T helper cells

When T helpers come in contact with antigen, they secrete compounds that co-stimulate B cells -> required for antibody production

Secrete compounds that activists Tk cells, in other worlds required for Tk activity

Secrete compounds that inhibit viral replication

Secrete compounds that attract phagocytes, compounds that attract + activate natural killer cells


HIV/AIDS *graph in notes

Kills of T helper cells

When T helper Coyne drops, can’t activate B cells (antibody production) because they are required for it

- about 75% in male homosexuals
- most of the rest -> IV drugs
- minorities
- females



Connective tissue
-> cells
-> non living matrix - plasma

Cells: formed elements
- erythrocytes (RBC’s)
- leukocytes (WBC’s)
- thrombocytes (platelets)


Hematological Analysis

Centrifuge blood
(dense material on bottom)

Plasma -> 53-59%

Buffy coat -> WBC’s and platelets (<1%)

Packed RBC’s
-> hematocrit
- percentage of whole blood occupied by
erythrocytes (not a count -> percentage*)

- males -> average 47%
- females -> average 41%


Red blood cell lifespan

Birth -> Erythropoiesis


- stimulated by erythropoietin to form->
(erythropoietin secreted by kidneys)

—divide by mitosis into->

-> synthesize hemoglobin
—-ejects nucleas (cell collapses)—>

Biconcave disc
—> reticulocyte

After two days ..
Reticulocyte —> erythrocyte


Red blood cell structure

Biconcave disc

A lot of hemoglobin


Primary function of erythrocytes

- carry oxygen around the body (because they contain hemoglobin)

- carry co2 around the body



-> globin (protein) + heme (contains iron)

(98.5% of all oxygen transported in the body is done so bound to hemoglobin)


Death of a red blood cell

A red blood cell lives for about 4 months/120 days

-> protein called spectrin - flexible

Narrow capillaries
-> spleen
- young rbc’s can fit through spleen
- old rbc’s are stiff and spleen tears them


Hemoglobin cycle
* see chart

Spleen -> rips up old rbc’s and releases free hemoglobin

Free hemoglobin engulfed by splenic macrophages

Macrophages broken into
-> heme
-> globin (free amino acids)

Heme -> liver

In liver, heme broken into iron and bilirubin
- iron is stored as ferritin or hemosiderin
(protein + iron)
- iron is transported as *transferrin in the blood

- bilirubin is secreted in bile -> small intestine
-> large intestine -> out in feces

Globin in blood
GI -> iron, amino acids, b12, b6, folic acid

Breakdown of RBC’s (heme, globin)
—> leads to decreased hematocrit

—> decreased hematocrit equals decreased oxygen carry capacity -> hyoxia*

Hypoxia (decreased oxygen in blood)
—> stimulates kidneys to secrete
erythropoietin which stimulates
red blood cell formation in bone


Normally (rbc’s)

Rate of RBC destruction
= rate of RBC formation

hypoxia for any reason stimulates an increase in erythropoiesis via an increase in EPO secretion
- aerobics
- COPO - chronic destructive pulmonary disorder
- anemia



- decreased oxygen carrying capacity of the blood
- decreased hematocrit, decreased hemoglobin concentration, or both

Types of anemia

1. Hemorrhagic anemia - bleeding
2. Aplastic anemia
- bone marrow problem
-> decreased RBC production, can’t
keep pace with RBC destruction
- leukemia
- drugs that treat cancer
- radiation poisoning

3. Deficiency anemias
- iron deficiency
- pernicious anemia
-> vit b12 deficiency
- b12 absorption require intrinsic factor
- intrinsic factor synthesized in gastric
- intrinsic factor deficiency

4. Hemolytic anemia
- abnormal high rate of RBC destruction that out paces production

- infection
- transfusion reactions
- abnormal hemoglobin
a.) sickle cell anemia)
-> (hemoglobin S)
- crystallizes ->
- rbc’s take in strange shapes
- cells become stiffer
- clog small blood vessels which
starve tissue down steam
b.) thalassemias
- produce fragile rbc’s that undergo
early destruction
-> results in hemolytic anemia