Physiology: Blood And Heart

Front 1

Functions of the blood:

Transports:

Protection:

Back 1

Oxygen, CO2, nutrients, waste,heat, and hormones

maintenance of normal Ph, normal body fluidvolume, hemostasis, fight infection, and maintainhomeostasis

Front 2

Blood turns red when:

and blue when:

hemoglobin is:

Back 2

hemoglobin binds with O2, hemoglobin binds with CO2

a pigmented protein in erythrocytes

Front 3

Plasma:

Buffy coat:

hematocrit:

a drop of blood outside the body separates into:

Back 3

55%, least dense, contains H2O, proteins, electrolytes, hormones, andnutrients

less than 1%, contains leukocytes, platelets

% RBC's, about 45%, most dense component

serum (plasma - fibrinogen) and clot (hematocrit plus fibrinogen) (reddish dense mass of cells)

Front 4

formed elements of blood:

The source of plasma water:

The source of plasma protein:

The source of blood cells:

Back 4

WBC, RBC, platelets

ingested H2O

liver

bone marrow

Front 5

Source of RBC formation:

Primary:

Secondary:

Tertiary:

Back 5

In adults, blood cells are formed by the red bonemarrow in the sternum, ribs,vertebrae, skull, and pelvis. 

Secondary: Blood cells can be formed by the marrow in thefemur & tibia (if necessary). 

Tertiary: In E.R. (excessive blood loss) blood cells can beformed in liver and spleen.

Front 6

Embryo primary RBC source:

RBC's lack _____ and do not perform _________

Back 6

liver and spleen

nuclei, mitosis during their short lifetime (120 days)

Front 7

RBC increases:

critical nutritional factors:

Hormone that stimulates RBC formation:

Back 7

afterexercising, after a largemeal, when a person is athigh altitudes, or whenbody temperature rises.

vitaminB-12, folic acid, and iron

Erythropoietin from thekidney stimulate RBCproduction from the bonemarrow.

Front 8

Blood prevents blood loss by:

Prevents infection by:

Back 8

Activating plasma proteins and platelets Initiating clot formation when a vessel is broken

Synthesizing and utilizing antibodies, Activating complement proteins, Activating WBCs to defend the body against foreign invaders

Front 9

anemia:

check notes - do I need to know each kind?

Back 9

a condition where the oxygen – carryingcapacity of blood is reduced due to RBC or hemoglobindeficiency, and result in lack of energy in the person

Front 10

leukocytes:

2 groups and their subcategories:

phagocytes and their subcategories:

Back 10

less than .1% of blood, generally function in lymphatic system

granulocytes (WBC that contain granules in theircytoplasm with their nuclei divide into lobes): Neutrophils, Eosinophils, Basophils

agranulocytes (lack granules): lymphocytes, monocytes

leukocytes that have the ability to engulf foreignsubstances for body defense purposes. These include the neutrophils, eosinophils, and monocytes

Front 11

Monocytes develop into ____, which:

Netruophils phagocytize:

Eosinophils:

Basophils:

Back 11

macrophages, travel long distances to find foreign substances

small particles in blood or connective tissue

control inflammation and allergic reaction

release anticoagulant (to prevent spontaneous blood clotting) and histamines to enhance inflammation

Front 12

monocytes

lymphocytes:

platelets =

and are critical in forming:

Back 12

phagocytize larger cells in connective tissues

attack foreign agents directly or indirectly by forming antibodies

thrombocytes, platelet plugs in hemostasis and blood clots with fibrinogen

Front 13

Albumin:

Globulin:

Fibrinogen:

Back 13

Albumin is critical in maintaining osmotic pressure in bloodand body fluids.

Globulin serves as protein transporters (e.g.for steroid hormones).

Fibrinogen is converted into fibrins inthe formation of a blood clot.

Front 14

plasma lipids combine with globulins to form:

VLDL:

LDL:

Back 14

lipoproteins

Very low density lipoproteins (VLDL) have a high amount oftriglyceride. It transports triglycerides synthesized in the liverfrom carbohydrates to adipose cells (bad cholesterol). 

Low density lipoproteins (LDL) have a high amount ofcholesterol . Delivers cholesterol to various cells, includingliver cells (bad cholesterol).

Front 15

HDL

Back 15

High density lipoproteins (good cholesterol)

Relatively high concentration ofprotein and low concentration of lipids.

Function: Transports to the liver remnants ofchylomicrons that have given up their cholesterol.

Note: A high ratio of HDL to LDL cholesterolappears to ward off plaque formation and heartdisease.

Front 16

Major events in red blood cell destruction

Back 16

1. Squeezing through the capillaries of active tissues damagesred blood cells.  2. Macrophages in the liver & spleen phagocytize damaged redblood cells.  3. Hemoglobin from the red blood cells is decomposed intoheme and globin.  4. Heme is decomposed into iron and biliverdin.  5. Iron is made available for reuse in the synthesis of new hemoglobin or is stored in the liver as ferritin.  6. Some biliverdin is converted into bilirubin.  7. Biliverdin and bilirubin are excreted in bile as bile pigments.

Front 17

Hormonal control of RBC steps:

Back 17

The kidney & liver tissue experience an O2deficiency.  These tissues release the hormone erythropoietin.  Erythropoietin travels to the red bone morrow and stimulates an increase in production of red cells.  As increasing number of red blood cells arereleased into the circulation, the O2 – carryingcapacity of blood rises.  The O2 concentration in the kidney and liver tissue increases, and the release of erythropoietin decreases.

Front 18

3 dietary factors affecting RBC production:

Back 18

vitamin B12, Iron, Folic acid

Front 19

B12 source and function:

Iron source and function:

Folic Acid source and function:

Back 19

source: Absorbed from small intestine.  Function: DNA synthesis. Requires intrinsic factor for absorption.

Absorbed from small intestine; conserved during red celldestruction and made available for reuse.  Function: Hemoglobin synthesis. Req. Vit. C

Absorbed from small intestine.  function: DNA synthesis.

Front 20

hemostasis:

Back 20

the stoppage of bleeding

Blood clotting involves a series of Rxs wherein each reactionstimulates the next Rx, which may be initiated by extrinsic orintrinsic mechanisms.

Clot formation depends on the balance between clotting factors that promote clotting and those that inhibit clotting.

Front 21

extrinsic and intrinsic mechanisms:

Back 21

The extrinsic clotting mechanism is triggered when blood contacts damaged tissue. Damaged blood vessels in the injuredarea release "tissue thromboplastin ", which after a series ofchemical reaction, produces "prothrombin activator "

The intrinsic clotting mechanism is triggered when blood contacts a foreign surface. blood being exposed to collagen fibersor other foreign substances after blood vessels are opened, willrelease the "Hageman factor", which will also produce the "pro-thrombin activator"

Front 22

Prothrombin activator

Back 22

"prothrombin activator " converts prothrombin (produced byliver) into thrombin, which in turn converts fibrinogen intofibrins. These steps require calcium and "clotting factors"(proteins that facilitate blood coagulation

Front 23

4 steps of blood clotting:

Back 23

1. Injury to wall of blood vessel

2. Vasoconstriction

3. Platelet Plug Formation

4. Clot formation

Front 24

Injury to wall of blood vessel:

Vasoconstriction:

Back 24

Injury (cut) to a blood vessel is followed by a series of reactionsthat result in the formation of a blood clot, which seals theinjured opening and prevents the loss of blood.

Adhesion of blood platelets to the exposed collagen fibers (inthe wall of the injured vessel) cause the release of serotoninfrom platelets, which induces strong vasoconstriction anddecrease blood flow.

Front 25

Platelet plug formation:

Back 25

contact of the platelets with collagen in the injuredwall releases thromboxane A2, which inducesaggregation of more platelets in the plug area andstimulates the formation of platelet pseudopods.These enable the platelet aggregates to bindtogether, forming a temporary plug to stop bloodloss (platelets adhere to rough surfaces and to eachother, forming a plug)

Front 26

clot formation:

Back 26

To strengthen the plug, Fibrinogen, a blood protein isconverted to fibrin; fibrin forms a net over the platelets. Red cells inthe center and exterior of the plug adhere to this net. The combinationof platelets and red cells entangled within a tight fibrin net forms ablood clot, a stronger and more permanent plug to stop blood loss

Front 27

see desktop for photo summary

Back 27

see other side

Front 28

To dissolve a clot:

Back 28

the enzyme plasmin lyses the fibrinnet; plasmin is formed from an inactive precursor, plasminogen

Front 29

4 clotting factors:

CHECK that we only need to know 4

Back 29

I . FibrinogenII. ProthrombinIII. Tissue ThromboplastinIV. Calcium

Front 30

6 factors that inhibit blood clot formation

Back 30

1. Smooth lining of blood vessel – prevents activation of intrinsicblood clotting mechanism.

2. Prostacyclin - inhibits adherence of platelets to blood vessel wall.

3. Fibrin threads - absorbs thrombin.

4. Antithrombin in plasma - interferes with the action of thrombin.

5. Heparin from mast cells and basophils - interferes with theformation of prothrombin activator.

6. Aspirin - inhibits prostaglandin production resulting in a defectiveplatelet release reaction.

Front 31

agglutination:

blood group is based on:

Order of popularity:

Back 31

clumping of erythrocytes when blood groups with different antigens and antibodies mix and bind

antigen presence

O, A, B, AB

Front 32

Antigens are synthesized during fetal development. About 2-8months after birth, the immune system will spontaneouslydevelop specialized proteins called antibodies to be"compatible" with these antigens

Back 32

see other side

Front 33

universal donor:

universal recipient:

Back 33

O

AB