chapter 19: the blood Flashcards

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1
Q

All cells need

A

nutrients and get rid of waste products

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2
Q

Body must maintain

A

homeostasis

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3
Q

Body fluids help in

A

connecting cells
– Intracellular fluid: cytoplasm
– Extracellular fluid: interstitial fluid, blood plasma, lymph, CSF

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4
Q

Two major networks help in connecting cells:

A

– Cardiovascular system: Heart, blood vessels, blood

– Lymphatic system: Lymphatic tissues/organs, lymphatic vessels, lymph

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5
Q

function of blood

A
  • Transportation : gases, nutrients, hormones, vitamins, wastes
  • Regulation : temperature, pH, water, minerals, nutrients
  • Protection : against diseases, loss of body fluids
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6
Q

characteristics of blood

A

thicker than water ( it has a greater viscosity)
constitutes 8% of body weight
in a human adult, there are 4-6 liters of blood
pH = 7.5- 7.45
blood is composed of a fluid portion called PLASMA and solid formed elements, called FORMED ELEMENTS. These formed elements are RED BLOOD CELLS, WHITE BLOOD CELLS AND PLATELETS

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7
Q

PLASMA

A
  • fluid portion of blood which consists 91% water and the rest, are solutes- electrolytes and proteins (albumin accounts for 58% of plasma proteins and it is important in the movement of water between the tissues and the blood), blood clotting proteins, wastes, nutrients and respiratory gases). Since plasma is the fluid portion of blood, it’s increase or decrease will be central in the volume of blood. Homeostatic mechanisms attempt to maintain blood at volume within a narrow limit -water intake through the digestive system closely matches water loss through the kidneys, lungs, digestive tract and skin.
  • Plasma composes 55% of whole blood
  • Plasma is a straw colored, clear liquid
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8
Q

FORMED ELEMENTS

A

cells and cell fragments. composes approximately 45% of whole blood
Red blood cells (RBCs) = erythrocytes
White blood cells (WBCs) = leukocytes
Platelets = thrombocytes

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9
Q

Hematocrit

measurement of % of RBCs in blood

A

females 39-45%

males 41-47%

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10
Q

Hemopoiesis

A

Blood cells are formed by a process called HEMOPOIESIS. In adults, hemopoiesis mostly
occurs in red bone marrow in the proximal humerus, femurs, the flat bones of the skull, sternum and ribs and the vertebrae and the pelvis (os coxae). Within the red bone marrow there are undifferentiated cells (stem cells) called HEMOCYTOBLASTS, which will give rise to RBCs, WBCs and Platelets.
It’s interesting to note that in children, hemopoiesis occurs in MOST bones. As a person gets
older, yellow bone marrow replaces red bone marrow.

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11
Q

Red blood cells ( RBCs)

A
  1. Compose more than 95% of formed elements.
  2. 4 days is required for the formation of a single RBC.
    3.–RBCs–are biconcave discs that will not have nuclei when they are mature and circulating.
    This absence of a nucleus: gives more room for them to hold HEMOGLOBIN = an oxygen carrying pigment.
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12
Q

Hemoglobin

A

Hemoglobin is made up of the protein GLOBIN bound to the red HEME pigment. The globin consists of 4 polypeptide chains each bound to a heme group. Each heme group contains an atom of iron in the center which bonds to oxygen. Each hemoglobin molecule can carry 4 oxygens. In each RBC there are 280 million hemoglobin molecules and therefore 1 billion molecules of oxygen
Remember that Vit B12 is necessary for red blood cell production and that this B12 comes from
the dietj absorbed into the circulation from the small intestine in the presence of Intrinsic Factor
(from stomach)

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13
Q

Structure and Function of RBCs

A

There is a close relationship between structure and function of RBCs.
a. The biconcave shape will result in increase surface area for gas diffusion AND gives the
cell more flexibility to fit through the small vessels.
b. Lack of a nucleus will allow for hemoglobin to fit in - therefore, more O2 can be carried.
Since there is no nucleus, no repair can occur, and about 120 days in males and 110 in
females, the RBC becomes fragile and either breaks or is phagocytized by the liver, spleen and
red bone marrow.

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14
Q

Production of RBCs

A

The process of RBC production is ERYTHROPOIESIS (erythropoiesis is a type of hemopoiesis).
Erythropoiesis occurs in steps within the red bone marrow.
The production of RBCs begins as all formed elements do, as hemocytoblasts. Some will divide
and differentiate into preerythroblasts which have nuclei, so hemoglobin can be synthesized.
Eventually, this developing cell ejects its nucleus, becoming a reticulocyte. The cell will now
have the biconcave shape due to the loss of the nucleus, allowing for more room for the
hemoglobin and therefore oxygen. These reticulocytes pass into the blood from the red bone
marrow. Under normal conditions, they develop into mature RBCs within 1-2 days after their
release into the blood.
Normally, 2.5 million RBC’s are produced/second. To maintain homeostasis, 2.5 million must be destroyed per second. The total amount of RBC’s circulating in 25 trillion in an adult.
Reticulocyte Count: The rate of erythropoiesis is measured by a reticulocyte count, hi health, older RBCs are replaced by new reticulocytes. It then will take 1-2 days for these reticulocytes to mature into fully functioning RBCs. Reticulocytes account for 0.5-1.5% of all RBCs in the blood sample

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15
Q

Erythropoiesis

A

is a type of hemopoiesis

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16
Q

Reticulocyte Count

A

The rate of erythropoiesis is measured by a reticulocyte count, In health, older RBCs are replaced by new reticulocytes. It then will take 1-2 days for these reticulocytes to mature into fully functioning RBCs. Reticulocytes account for 0.5-1.5% of all RBCs in the blood sample.

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17
Q

Homeostasis and RBCs - erythropoietin.

A

The number of RBCs that are circulating must be kept constant. The body maintains this level by
ERYTHROPOIETIN, a hormone that controls erythropoiesis.

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18
Q

erythropoietin

A

Hormone that is released by the kidneys that will stimulate the red bone marrow to increase the production of RBC. The direct stimulus is HYPOXIA (lack of adequate O2 to the tissues.) This hypoxic state can be caused by different situations like a decrease in RBCs (hemorrhage) or a respiratory illness (pneumonia or emphysema).
Renal failure patients may lack erythropoeitin and therefore suffer a low hct, often one half the
normal level. RECOMBINANT ERYTHROPOIETIN can be given.

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19
Q

RBC LIFE SPAN

A

RBCs can only live for 110 - 120 days due to the lack of the nucleus and therefore their inability to produce new proteins. When they are removed from circulation and destroyed, the breakdown products are recycled.
Macrophages (type of WBC that is a phagocyte) located in the SPLEEN, LIVER and RED BONE MARROW take up the ruptured RBCs. The lysosomes within these macrophages digest the hemoglobin , reducing it to globin, iron and bilirubin

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20
Q

Hemoglobin from ruptured RBC’s is broken down into:

A

GLOBIN: This is a protein which will eventually be broken into AMINO ACIDS and used by cells in protein synthesis.
IRON: This is released, taken to red bone marrow and recycled into hemoglobin as new RBC’s are formed.
BILIRUBIN: This is the breakdown product of heme caused by degradation of RBC’s in the liver, where it becomes part of the bile and thus gives bile it’s yellow color. Bilirubin is released into the plasma, where it binds to ALBUMIN and transported to liver. It eventually become part of BILE, a product of the liver.
This bile will be stored in the GALLBLADDER, eventually released into the small intestine become part of the chime and give the feces their characteristic color. Some of the bile will be absorbed from the intestine into the blood, modified by the kidney and excreted into urine, giving the urine its characteristic color

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21
Q

JAUDICE

A

is the yellow color that is seen in the skin and sclerae of the eyes. It iscaused by a buildup of bilirubin in the circulation and within the interstitial spaces.

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22
Q

PATHOLOGY OF RBCs

A decrease in the number of RBC’s can lead to pathology, as can an increase in these cells.

A

Anemia
Condition of reduced oxygen-carrying ability in the blood. Symptoms: fatigue, pale, cold. There are different types of anemia.

23
Q

Hemorrhagic anemia

A

blood loss -> decrease number of RBCs

24
Q

Hemolytic anemia

A

RBCs rupture prematurely -> decrease # of RBCs (parasistes, transfusion of mismatched bld)

25
Q

Aplastic anemia

A

Pathology of the red bone marrow (not just RBC) leading to low RBC count or malformed RBCs. Cause can be cancer, radiation, drugs

26
Q

Dietary anemia

A
  • Not enough iron in bld to carry enough O2. Iron is necessary in the production of hemoglobin
27
Q

Pernicious anemia

A

this type of anemia is due to a lack of INTRINSIC FACTOR in the stomach.
I.F. is needed for absorption of vit B12 in the small intestine. B12 is needed for the red bone marrow to produce erythrocytes. As a person ages, there may be a decrease in the production of intrinsic factor.
Decrease in I.F -> decrease in # of RBC-> decrease in amount of O2 to tissues

28
Q

Sickle Cell Anemia

A

genetic disease in which the RBC looses its round shape and sickles. This will lead to less O2 going to the tissues, and pain will occur. Mostly seen in people with African heritage

29
Q

RBCs increase

A

Not only is it dangerous to have too little the amount of RBCs but too many will cause difficultly.

30
Q

RBCs increase - Polycythemia

A

A: Abnormal increase of RBCs-> increase viscosity of blood -> slows down flow ->decrease rate of oxygen getting to tissues. Occurs when hcL= 65% and above. Why would this occur? If there is a situation of constant chronic hypoxia, polycythemia can result. Seen with EMPHYSEMA, a chronic respiratory problem.

31
Q

Blood Doping

A

: Practiced by some athletes. The individual’s blood is drawn and stored. The RBCs are then transfused into the person right before the competition. The increased number of RBCs-> increase O2 to tissues. This is considered illegal.

Another illegal practice is the use of recombinant erythropoietin by athletes before a race. Especially dangerous in sports that cause dehydration, which leads to a higher abnormal hct. Seen in biking competition (Tour de France). Also see an increase in RBCs if go to a higher altitude.

The increase in RBC’s is also seen in normal situations, as when the individual goes to a higher altitude, where there is less oxygen available, hi this case, with time, the body will increase its number of RBCs in order to maintain the needed level of oxygen to the tissue

32
Q

Leukocytes - White Blood Cells ( WBCs)

A

Unlike RBCs, WBCs are nucleated cells that do not contain hemoglobin. They are important in DEFENSE of the body against invaders (viruses, bacteria, toxins, parasites etc.) There are many
more RBCs than WBCs ( 700:1) and they, as well as RBCs and platelets, are formed within red
bone marrow.

33
Q
  1. There are 2 general types of WBCs: granular and agranular
A

a. granular WBCs - these are cells that have 1 LOBED NUCLEUS within them, and
have granules within the cytoplasm. They are: NEUTROPHILS, EOSINOPHILS and
BASOPHILS.
b. agranular WBCs - These WBCs do not have observable granules in the cytoplasm.
Their nuclei ( 1 per cell) are large but not lobed. The 2 types are LYMPHOCYTES and
MONOCYTES.

34
Q

LEUKOCYTOSIS

A
  1. Ordinarily, most WBCs live for a few days. The notable exception is some lymphocytes that
    can live for months or years. The number of WBCs will increase when there is an infection. This is a NORMAL PROCESS and is called UKOCYTOSIS. The body is continually challenged by viruses and bacteria. If they are able to cross the skin and the mucous membranes and get into deeper tissue, the WBCs will attempt to destroy them by hagocytosis or immune response
35
Q

DIAPEDISIS

A
  1. The WBCs must leave the bloodstream and get into the infected tissue. Most will do their
    duty within the infected area and die, never returning to the blood. The movement of WBCs from blood into tissues is termed DIAPEDISIS.
    DIAPEDISIS: Process in which WBCs leave the blood. They slow down, roll over the endothelial cells and then squeeze between the cells of the capillaries, out of the vessel.
36
Q

CHEMOTAXIS.

A

The WBCs are attracted to the injured area by chemicals that are released by the injured tissue.
This is called CHEMOTAXIS.
Chemotaxis: Attraction of phagocytes to microbes by chemical stimulus

37
Q

Bacteria infection processing

A

During a bacterial infection, Neutrophils are first on the scene, reaching the infected area by
chemotaxis and diapedisis and destroying the pathogen (invader) by phagocytosis.Monocvtes will arrive later on in the infection, but will appear in a large number and continue to destroy more icrobes. Monocytes will enlarge and differentiate into MACROPHAGES. and then phagocytize the invaders. These WBCs are also active in cleaning up the debris of dead cells after the infection is over. The other types of WBCs are also involved with protection of the body, depending upon the type of pathogen. Leukocytosis indicates infection or inflammation. The type of WBC involved can be detected by a differential WBC count.

38
Q

Neutrophils

A
  • 60-70 % in blood and description
  • lobed nucleus, granules in cytoplasm
  • tissue developed in red bone marrow
  • function: phagocytosis of bacteria and fungi
39
Q

Eosinophils

A
  • 2-4% in blood and description
  • lobed nucleus, rad granules in cytoplasm
  • tissue developed in red bone marrow
  • function: phagocytosis of parasitic worms
40
Q

Basophils

A
  • 0.5 - 1.0% in blood
  • lobed nucleus, granules
  • tissue developed in red bone marrow
  • function: releases heparin and histamines which cause an increase in the inflammatory response. Enter tissues by diapedisis
41
Q

Lymphocytes

A
  • 20 - 25% in blood
  • compact nucleus, no visible granules in cytoplasm
  • tissue developed in red bone marrow and lymphoid tissue
  • function: immune response (antibody production)
42
Q

Monocytes

A
  • 3-8% largest WBC in size kidney shaped nucleus, no visible granules in cytoplasm
  • tissue developed in red bone marrow and lymphoid tissue
  • fuction: can enter tissues and become larger = MACROPHAGES can then go through phagocytosis of foreign material
43
Q

Pathology of WBCs

A
  • infectious mononucleosis
  • Leukemia
  • Leukopenia
44
Q

Infectious mononucleosis

A

A contagious disease characterized by high count of abnormal and large lymphocytes (originally thought to be monocytes due their size). Caused by the Epstein-Barr virus.

45
Q

Leukemia

A

Malignant disease of blood forming tissues characterized by uncontrolled production of WBCs . So many of these abnormal WBCs are produced that there will be a DECREASE in the production of RBCs and platelets. Anemia and clotting difficulties follow.
Possible treatments: radiation, chemotherapy, bone marrow transplants and transplantation of umbilical cord blood

46
Q

Leukopenia

A

Decrease in the number of WBCs - often due to chemotherapy, radiation therapy, viruses, some tumors,..

47
Q

Platelets

A
Hemocytoblasts will also differentiate into MEGAKARYOCYTES which will eventually
become PLATELETS (thrombocytes). These are FRAGMENTS of cytoplasm of the megakaryocytes that will be released into the blood. They do not have a nucleus, are normally small and round in shape and will only live about 5-9 days. Platelets are capable of forming PLATELET PLUGS that can seal small breaks in blood vessels
48
Q

Hemostasis and platelets

A

The volume of blood must be kept constant in a person, and loss of blood due to a trauma
is dangerous. Hemostasis is a homeostatic process that will stop the loss of blood. Normally, blood flows smoothly in vessels as long as the endothelium (lining of vessels) is unbroken. BUT, if a blood vessel wall breaks, a whole series of reactions is set in motion to accomplish HEMOSTASIS = stoppage of bleeding. There are 3 Phases of HEMOSTASIS. and they occur in rapid sequence:
a. Vascular Spasms
b. Platelet Plug Formation
c. Coagulation (blood clotting)
As long as the injury is not too great, blood loss can be prevented when the clot finally seals the
damaged vessel wall.

49
Q

VASCULAR SPASM

A

The immediate (but temporary) response to blood vessel injury is the CONSTRICTION of the
smooth muscle of small blood vessels that has been injured. This will decrease the amount of
blood that can be lost and will last a few minutes to a few hours. During this time, the
PLATELET PLUG will form and coagulation will occur:
This is a localized reaction.

50
Q

PLATELET PLUG FORMATION

A

Platelets play a key role in hemostasis by forming a plug that temporarily seals the break in the vessel wall. These platelets will also stimulate the events that will lead to a blood clot forming.
Normally, platelets are round and smooth and do not stick to each other or to the smooth endothelial lining of the vessels. However, when the ndothelium is damaged, the platelets in the blood flowing by the injury go through many changes. They swell and their membranes change and become sticky and begin to adhere to each other. They release PROSTOGLANDINS, CALCIUM, PLATELET PROTEINS and ENZYMES that promote chemotaxis, attracting more platelets to collect in injured area. PLATELET ADHESION occurs, when platelets stick to each other and to the exposed collagen within the walls of the injured blood vessels. Most of this adhesion occurs because of von WILLEBRAND FACTOR (yWF), a protein produced and secreted by the blood vessel, forming bridges between the platelets and the collagen found within the vessel wall. Due to a series of reactions, more platelets collect at the site, release
chemicals by exocytosis. These activated platelets change shape, form FIBRINOGEN.
RECEPTOR that will be able to bind with FIBRINOGEN, a plasma protein that is crucial to
hemostasis. Within 1 minute a PLATELET PLUG is formed.
ASA( aspirin) will inhibit the prostaglandins from being released and therefore can inhibit PP formation. A person before surgery is told not to use ASA.

51
Q

COAGULATION

A

Vascular spasm and platelet plugs are not enough to stop bleeding from larger cuts. Coagulation
is also necessary for more extensive damage. During coagulation, a clot is formed in the injured
area. A BLOOD CLOT is a network of threadlike protein fibers (FIBRIN) that traps blood cells,
platelets and fluid. The formation of a clot is dependant upon the existence of COAGULATION
FACTORS circulating within the blood plasma. When not needed, these factors are in an INACTIVE state and won’t trigger clotting. In response to an injury however, the clotting factors
are activated and a clot is formed. This activation is complex, involving a variety of substances,
includingi-jcalcium ions (CAW-)

52
Q

The Activation of Clotting Proteins occurs in 3 main stages

A

Stage 1: Formation of Prothrombinase
Referring to the cascade on p. 665, note that the enzyme PROTHROMBINASE can be formed by 2 separate pathways - the EXTRINSIC PATHWAY and the INTRINSIC PATHWAY.
EXTRINSIC PATHWAY: It begins with chemicals outside (EXTRINSIC ) of the blood. The damaged tissue releases TISSUE FACTORS that in the presence of Ca++ will stimulate the formation of PROTHROMBINASE.
INTRINSIC PATHWAY: This pathway begins inside (INTRINSIC) of the blood vessels. The damaged walls of the vessels will expose collagen and connrective tissue. Again, in the presence of Ca++, PROTHROMBINASE is formed.
These 2 pathways stimulate each other.
Once PROTHROMBINASE is formed by the 2 pathways, Stage 2 and 3 can occur.

Stage 2: Conversion of Prothrombin to Thrombin
Stage 3: Conversion of Fibrinogen to Fibrin
These insoluble fibrin strands that result in stage 3 will glue the platelets together and make the
basis of the clot. This web-like structure will trap formed elements inside of it and clot formation is normally completed within 3 -6 minutes after damage to the vessel.

53
Q

What is the connection between Vit K and clotting

A

clotting

54
Q

What are the 2 sources of vit K

A

Diet and