Blood Flashcards (my version)

Functions of blood:

Transports: O2, CO2, Nutrients, hormones, wastes

Regulates: Body temp, pH in body tissues, fluid volume (ex: salts)

protection: protects against blood lost and disease

What is the pH of blood

7.35-7.45

Composition of blood:

• is denser that H2O

• temp: 100.4 F (38 C)

• constitutes 8% of body wright and 4-5 liters in avg adult

What is normal body temp and what structure regulates it?

37C (98.6F), hypothalamus

Composition of blood—Plasma components:

• 90% H2O with dissolved compounds

• is 55% of whole blood

• least dense component

• has proteins: albumin, antibodies, clotting proteins

  • their function: maintain osmotic pressure

• electrolytes: Na, K, Ca, Mg, Cl, bicarbonate

What are the formed elements

RBCs, Leukocytes, Platelets

(45% of whole blood)

• only WBCs are complete cells (RBC have no nuclei/other organs, platelets=cell fragments)

• most formed elements survive in blood stream for a few days

• most blood cells originate in red bone marrow and don’t divide

What is hematocrit

% of blood volume that is RBCs

normal values:

• men: 40-54%

• women: 36-48%

Where are WBCs and platelets located

• buffy coat (<1%)

• is a thin whiteish layer btw RBCs and plasma layer

Components of Plasma- Albumin

• 60% of plasma proteins

• transports substances (bilirubin, bile salts, T4/T3

Components of plasma—globulins

• α (alpha), β (beta) transport hormones, cholesterol and iron

• gamma globulins= antibodies (immunoglobulins)

Components of plasma—fibrinogen

• precursor for the clotting protein fibrin

How many microliters are there of RBCs (erythrocytes)

4.8-5.4 million/μL

How many microliters are there of WBCs (leukocytes)

4500-11000μL

What are the granulocytes and their percentages of WBCs

1. neutrophils 60-70% of WBCs

2. eosinophils: 2-4% of WBCs

3. Basophils: 0.5-1%

What are the agranulocytes and their percentages of WBCs

1. lymphocytes: 20-25% of WBCs (contains T and B lymphocytes and natural killer cells)

2. monocytes 3-8%

How many microliters are there for platelets

150,000–400,000/ μL (microliter)

erythrocytes facts:

• biconcave shape

• no nucli/organelles

• lasts 120 days and is then destroyed by spleen or liver

What are the enzymes in the cytoplasm of RBCs

• glycolytic enzymes to carry out glycolysis

• carbonic anhydrase—converts CO2 to HCO3

What 3 features make efficient gas transportation for RBCs

1. their biconcave shape—offers huge surface area relative to volume for gas exchange

2. hemoglobin makes up 97% cell volume (not accounting H2O)

3. RBCs have no mitochondria

   • ATP production is anaerobic, they don’t consume the O2 they trasnport

why are red blood cells red

Hemoglobin is made of two main parts: the "heme" group and the "globin" group. The heme group contains iron which gives the red color to the red blood cell. The globin group is a protein that helps the red blood cell carry and hold oxygen in place as it moves throughout the body.

what is the function of erythrocytes

• transport oxygen (O2) and to a lesser extent carbon dioxide (CO2)

• contains hemoglobin (Hb/Hgb)

• each RBC contains 250 million Hb molecules

• O2 loading in the lungs

  • produces oxyhemoglobin (ruby red)

• O2 unloading in tissues

  • produces deoxyhemoglobin/reduced hemoglobin (dark red)

• CO2 loading in tissues

  • 20% of CO2 in blood binds to Hb, producing carbaminohemoglobin

what is hemoglobin made up of

• 4 globin polypeptide and 4 heme groups

• a heme pigment is bonded to each globin chain

  • each heme’s central iron atom binds one O2

• each Hb molecule can transport four O2

• each RBC contains 250 million Hb molecules

What is erythropoiesis?

production of new RBCs (~3 million/sec)

occurs in red bone marrow

rate of production is controlled by erythropoietin (EPO) that is produced by the kidneys in response to blood oxygen levels

What is hematopoiesis

all blood cells arise from a common stem cell found in red bone marrow

what is the formation of erythropoiesis?

1. hemocytoblast—> reticulocyte ~15 days

2. reticulocyte—> matures in bloodstream ~2 days

   • is controlled by erythropoietin

What is the the consequences of using artificial EPO

• the use of EPO increases hematocrit, allows athletes to increase stamina and performance

• increases hematocrit from 45-65% w/ dehydration concentrating blood even more

• blood becomes like sludge and can cause clotting, stroke or heart failure

What are the dietary requirements for erythropoiesis

• amino acids, lipids, carbs

• iron (available from diet)

• vitamin b12 and folic acid

  • necessary for DNA synthesis for rapidly dividing cells (such as developing RBCs)

what is the fate and destruction of erythrocytes

1. life span: 100-120 days

2. RBCs are anucleate, cannot synthesize new proteins, grow or divide

3. old RBCs are fragile, Hb begins to degenerate

4. can get trapped in smaller circulatory channels, especially spleen

5. macrophages in spleen engulf and breakdown dying RBCs

What are 2 types of blood loss (erythrocyte disorders)

1. acute hemorrhagic anemia

   • rapid blood loss

2. chronic hemorrhagic anemia

   • slight but persistent blood loss

   • primary problem must be treated to stop blood loss

What is Iron-deficiency anemia

• not enough RBCs being produced

• Can be caused by hemorrhagic anemia, but also by low iron intake or impaired absorption

• RBCs produced are called microcytes

• Small, pale in color

• Cannot synthesize hemoglobin because there is a lack of iron

  Treatment: iron supplements

What is pernicious anemia

• not enough RBCs being produced

• Autoimmune disease that destroys stomach mucosa that produces intrinsic factor

• Intrinsic factor needed to absorb B₁₂

• B₁₂ is needed to help RBCs divide

• Without B₁₂ RBCs enlarge but cannot divide, resulting in large macrocytes

Treatment: B₁₂ injections or nasal gel

What is renal anemia

• cause: lack of EPO

• often accompanies renal disease

  • kidneys can’t produce enough EPO

• treatment: synthetic EPO

what is aplastic anemia

—Destruction or inhibition of red bone marrow

—Can be caused by drugs, chemicals, radiation, or viruses

—Usually cause is unknown

—All formed element cell lines are affected

—Results in anemia as well as clotting and immunity defects

—Treatment: short-term with transfusions, long-term with transplanted stem cells

what is sickle cell anemia

—Hemoglobin S: mutated hemoglobin

—Only 1 amino acid is wrong in a globin beta chain of 146 amino acids

—RBCs become crescent shaped when O₂ levels are low

—Example: during exercise

—Misshaped RBCs rupture easily and block small vessels

Results in poor O₂ delivery and pain

what is polycythemia

—Abnormal excess of RBCs; increases blood viscosity, causing sluggish blood flow

—Polycythemia vera: Bone marrow cancer leading to excess RBCs

—Hematocrit may go as high as 80%

—Treatment: therapeutic phlebotomy

—Secondary polycythemia: caused by low O₂ levels (example: high altitude) or increased EPO production

What are leukocytes and their function

• protects against infection and initiates inflammation

• destroys cancerous cells

• tissue repair

What are granulocytes and the 3 diff types of them

• granulocytes- granule containing cells w/ lobed nuclei

• neutrophils (60-70%)'

  • phagocytes

  • first on the scene of infection and triggers inflammation

• eosinophils (1-4%)

  • associated with allergies and parasite infections

• basophils (<1%)

  • contain and release histamine

  

What are the 2 types of agranulocytes

• monocytes (2-6%)

  • travel into the tissue and mature into macrophages

• lymphocytes (25-33%)

  • specific immune defenses

  • B, T and NK cells

what is a mnemonic to remember decreasing abundance in blood

Mnemonic to remember decreasing abundance in blood: Never let monkeys eat bananas (neutrophils, lymphocytes, monocytes, eosinophils, basophils)

What is leukopenia

• abnormally low WBC count

  • can be drug-induced, particularly by anticancer drugs or glucocorticoids

what is leukemia

• overproduction of abnormal WBCs

  • Usually involve clones of single abnormal cell

• Named according to abnormal WBC clone involved

• Myeloid leukemia involves myeloblast descendants

  Lymphocytic leukemia involves lymphocytes

• Acute (quickly advancing) leukemia derives from stem cells

• Primarily affects children

• Chronic (slowly advancing) leukemia involves proliferation of later cell stages

• More prevalent in older people

• Without treatment, all leukemias are fatal

• Immature, nonfunctional WBCs flood bloodstream

• Cancerous cells fill red bone marrow, crowding out other cell lines

• Leads to anemia and bleeding

• Death is usually from internal hemorrhage or overwhelming infections

• Treatments: irradiation, antileukemic drugs; stem cell transplants

What are platelets

• aka thrombocytes

• irregular shaped cell fragment from megakaryocytes

• play role in blood clotting

• normal blood contains 150,000-400,000 platelets/microliter

What is hemostasis

• prevents the loss of blood when blood vessels are damaged

• requrires clotting factos and substances released by platelets and injured tissues

• 3 phases that occur at the same time:

  • vascular spasm

  • platelet plug formation

  • coagulation

Detailed steps of hemostasis (step 1)

vascular spasms:

• vessel responds to injury with vasoconstriction

• vascular spasms are triggered by:

  • direct injury to vascular smooth muscle

  • chemicals released by endothelial cells and platelets

  • pain reflezes

  • most effective in smaller blood vessels

Detailed steps of hemostasis (step 2)

—Platelets stick to collagen fibers that are exposed when vessel is damaged

—Platelets do not stick to intact vessel walls because collagen is not exposed

—Also prostacyclins and nitric oxide (NO) secreted by endothelial cells act to prevent platelet sticking

—Platelet plug formation

• Damaged blood vessels cause platelets to become sticky and cling to the site

• These platelets release chemicals that:

• Attract other platelets

• Cause vasoconstriction

• —When not damaged, normal endothelial cells release prostacyclin and NO to inhibit platelet aggregation

Detailed steps of hemostasis (step 3)

coagulation

• is the clotting cascade

  • involves 13 clotting factors

  • requires Ca2+ presence

  • summary of events:

    • An initial inactive clotting factor, found in the plasma, is activated by exposed collagen

    • This activates the next factor and so on….. Until thrombin converts fibrinogen into fibrin

What are the intrinsic and extrinsic pathways

intrinsic:

• initiated when Hageman factor is activated by exposed collagen

extrinsic:

• Factor X is activated by thromboplastin released by damaged tissues

What is the role of thrombin in the clotting cascade

—Converts fibrinogen to fibrin

—Activates stabilizing factor (XIII)

—Enhances conversion of more thrombin from prothrombin

—Enhances platelet aggregation

What is clot retraction

platelets rtapped in the clot contract and squeeze serum out

what is vessel repair

platelets attract fibroblasts that repair blood vessel

what is clot dissoultion

urokinase and tissue plasminogen activator (tPA) converts plasminogen into plasmin which breaks down fibrin

what are 2 major types of hemostasis disorders

• thromboembolic disorders:

  • results in undesirable clot formation

• bleeding disorders:

  • abnormalities that prevent normal clot formation

what is the difference between thrombus, embolus and embolism (thromboembolic conditions)

—Thrombus: clot that develops and persists in unbroken blood vessel

—May block circulation, leading to tissue death

—Embolus: thrombus freely floating in bloodstream

—Embolism: embolus obstructing a vessel Example: pulmonary or cerebral emboli

—Risk factors: atherosclerosis, inflammation, slowly flowing blood or blood stasis from immobility

what are some drugs to help/cure thromboembolic conditions

—Anticoagulant drugs: used to prevent undesirable clotting

—Aspirin: lowers heart attack incidence by 50%

—Heparin: used clinically for pre- and postoperative cardiac care as well as to prevent venous thrombosis

—Warfarin: reduce risk of stroke in patients prone to atrial fibrillation

what is thrombocytopenia

—deficient number of circulating platelets

—Petechiae appear as a result of spontaneous, widespread hemorrhage

—Due to suppression or destruction of red bone marrow (examples: malignancy, radiation, or drugs)

—Platelet count <50,000/μl is diagnostic

Treatment: transfusion of concentrated platelets

what is hemophilia

—Includes several similar hereditary bleeding disorders

—Hemophilia A: most common type (77% of all cases) due to factor VIII deficiency

—Hemophilia B: factor IX deficiency

—Hemophilia C: factor XI deficiency, milder

—Symptoms include prolonged bleeding, especially into joint cavities

—Treatment: injections of genetically engineered factors; has eliminated need for plasma transfusion.

Restoring blood volume

—Death from shock may result from low blood volume

—Volume must be replaced immediately with

—Normal saline or multiple-electrolyte solution (Ringer’s solution) that mimics plasma electrolyte composition

—Replacement of volume restores adequate circulation but does not replace oxygen-carrying capacities of RBCs

transfusing RBCs

—Whole-blood transfusions are used only when blood loss is rapid and substantial

—Infusions of packed red blood cells, or PRBCs (plasma and WBCs removed), are preferred to restore oxygen-carrying capacity

—Blood banks usually separate donated blood into components; shelf life of blood is about 35 days

—Human blood groups of donated blood must be determined because transfusion reactions can be fatal

—Blood typing determines groups

how many blood types are there?

8

• A-

• A+

• B-

• B+

• AB-

• AB+

• O-

• O+

What antigens and antibodies do the blood types have in their plasma

• A-: A antigen , Anti-B antibody

• A+: A antigen, Anti-B antibody

• B-: B antigen, Anti-B antibody

• B+: antigen, Anti-B antibody

• AB-: BOTH A and B antigens, NEITHER antibody

• AB+: BOTH A and B antigens, NEITHER antibody

• O-: NEITHER A nor B antigen, BOTH anti-A and anti-B antibodies

• O+:NEITHER A nor B antigen, BOTH anti-A and anti-B antibodies

what blood type is the universal recipient

AB+

What blood type is the universal donor

O-

What is agglutinogens

agglutinogens= antigens

• are antigens on the surface of red blood cells

what are agglutinins

agglutinins= antibodies

• Agglutinins are antibodies in the plasma

Agglutination Reaction of ABO Blood-Typing with Antisera

Anti-A Serum	Anti-B Serum	Blood Type
Agglutination	No Agglutination	Type A
No Agglutination	Agglutination	Type B
Agglutination	Agglutination	Type AB
No Agglutination	No Agglutination	Type O

Explain Hemolytic disease of the newborn and the rationale for treatment

• a condition in which a Rh- mother who was previously sensitized by a blood transfusion or a previous Rh+ pregnancy carries a fetus who is Rh+ and the mother’s anti-Rh antibodies enter the fetus’s circulation

• this causes agglutination and hemolysis of the fetus’s RBCs

• Treatment for this condition is to remove the fetus’s Rh+ blood and replace it with Rh- blood from an unsensitized donor to lower the level of anti-Rh antibodies.