Chapter 17 Blood and Hematology Flashcards

1
Q

Blood and 3 Elements It’s Composed of:

A

A fluid connective tissue composed of:
o Plasma: non-living fluid matrix that is 90% water plus dissolved solutes.
o Formed Elements are the living blood cells:
o Erythrocytes: Red Blood Cells
o Leukocytes: White Blood Cells
o Thrombocytes: Platelets which are pieces of cells

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2
Q

Hematocrit:

A

The amount of red blood cells in blood or percent blood volume of RBC’s.
o Typically 47% + or – 5% for males and 42% + or – 5% for females.

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3
Q

Physical Characteristics and Volume of Blood:

A

o Blood is a sticky, opaque fluid with a metallic taste (iron).
o Color is scarlet (oxygen rich) to dark red (oxygen poor).
o Osmolarity: 280-296 mOsm/L= the concentration solute or particles in a given volume of solution. The number of particles translates to the ability to attract H2O
o pH 7.35-7.45, or alkaline
o 38 degrees C (100.4 degrees F)
o ~8% of body weight.
o Average volume: 5-6 L for males and 4-5 L for females.

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4
Q

Ways of Withdrawing Blood:

A

o Venipuncture: Shoot for antecubital region ( Median cubital vein). Walls of veins are thinner. Blood pressure is lower in veins than arteries.
o Arterial Puncture: To measure blood gases.
o Capillary Sticks: Fingers, Ear Lobes, Heel. (For Diabetics)

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5
Q

Functions of Blood:

Transport of

A

o O2 and nutrients to body cells.
o Metabolic Wastes to lungs (CO2) and kidneys (uric acid) for elimination.
o Hormones from endocrine organs to target organs.
o Certain blood proteins transport fats and cholesterol.

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6
Q

Functions of Blood:

Regulation of

A

o Body Temperature: by absorbing and distributing heat (vasodilation/vasoconstriction of BVs) through blood shunting.
o Normal pH (7.35-7.45) using buffers (from solutes in blood).
o Adequate fluid volume in circulatory system ( blood proteins and salts keep fluid within blood vessels due to osmolarity=water wants in?)

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7
Q

Functions of Blood:

Protection Against

A

o Blood Loss: Plasma proteins (fibrinogen) and platelets initiate clot formation.
o Infection: Antibodies, Complement proteins (initiate and enhance the inflammatory response and work with antibodies against antigens), and WBCs/Leukocytes (defend against foreign invaders).

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8
Q

Components of Blood Plasma:

A

o Blood plasma contains plasma proteins ( 8% of blood plasma) that are 90% produced by the liver
o Blood plasma is 90% water by volume with over 100 substances dissolved in it (straw color) =
o 1) 60% Albumin (3.5 – 5.4g/dl = protein made in liver & major contributor to blood osmotic pressure, blood buffering, and blood viscosity
o > too large to move out of the blood vessels à creates osmotic pressure gradient inside the blood vessels
o > transport fatty acids, hormones, ions and nutrients, Vita D, bilirubin
o 2) 36% Globulins
o > Alpha & Beta globulins made in the liver for transport of iron, lipid, fat
o > Gamma globulins (or immunoglobulins) = are antibodies & made by plasma cells not liver (differentiated WBC)
o 3) 4% Fibrinogen = made in liver and essential in blood clotting (hemostasis)
o 4) Nitrogen by-products of metabolism—lactic acid, urea, creatinine.
o 5) Nutrients—glucose, carbohydrates, amino acids
o 6) Electrolytes—Na+, K+, Ca2+, Cl–, HCO3 for normal osmotic pressure and pH
o 7) Respiratory gases—O2 and CO2
o 8) Regulatory proteins such as hormones, enzymes

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9
Q

Hypoproteinemia:

A

o Causes: Extreme starvation, diets severely deficient in protein, liver disease interfering with protein synthesis, kidney disease that allows proteins to leak from blood into the urine, severe burns, severe trauma.
o Consequences: Decreased osmolarity of blood (blood doesn’t attract to water as much, water diffuses into the interstitial spaces between cells), edema= excess fluid in interstitial spaces, and ascites= excess fluid in peritoneal cavity.

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10
Q

Erythrocytes (Red Blood Cells):

A

o Biconcave discs, anucleate, essentially no organelles.
o Filled with hemoglobin for gas transport.
o Contain the plasma membrane spectrin and other protein.
o Spectrin: Provides flexibility for RBCs to change shape as necessary to fit through the smallest capillary.
o RBC’s are the major factor contributing to blood viscosity.
o Structural characteristics contribute to gas transport both O2 to tissues and CO2 to lungs
o Biconcave shape—huge surface area relative to volume where cytoplasm is close to cell surface
o >97% hemoglobin (not counting water)
o Plasma membrane have antigens (glycoproteins/lipids) on surface which determines different blood groups (A, B, AB,O) and Rh factor.
o Men have more RBC’s than women
o No mitochondria; ATP production is anaerobic; no O2 is used in generation of ATP (RBC’s don’t’ steal oxygen away for themselves!!)
o HbA1-C test: measures amount of glucose sticking to erythrocyte during its’ 3 month lifetime…should be less than 7%

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11
Q

Functions of Erythrocytes:

A

o One Hemoglobin (Hb) molecule is made up of:
o 1) Protein globin = four polypeptide chains (2 alpha and 2 beta chains)
o 2) Four heme (red pigment) groups bonded to protein globin chains
o An iron atom is centered in each heme group: each heme group can bind to one O2 molecule
o So, each Hb molecule can transport four O2
o Each erythrocyte contains 250 million molecules of Hb
o Number of O2 molecules held by each RBC = 250 million Hb X 4 O2= 1 billion O2 molecules carried per erythrocyte

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12
Q

Hemoglobin:

A

o O2 loading in the lungs: Produces oxyhemoglobin (ruby red)
o O2 unloading in the tissues: Produces deoxyhemoglobin or reduced hemoglobin (dark red, port wine)
o CO2 loading from the tissues: Produces carbaminohemoglobin (carries only 20% of CO2 in the blood)

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13
Q

Hematopoiesis/Hemopoiesis:

A

o Hematopoiesis (or hemopoiesis) is blood cell formation of RBCs, leukocytes, thrombocytes (*called the formed elements)
o Before birth: this occurs in the yolk sac, liver, spleen, thymus, lymph nodes
o After birth: red bone marrow = sternum, ribs, clavicle, scapula, illium of os coxae, vertebrae, and proximal epiphyses of humerus and femur.
o Hemocytoblasts are hematopoietic which are stem cells which are in the red bone marrow
o Gives rise to all “formed elements” = erythrocytes, leukocytes (WBCs), and thrombocytes (platelets)
o Hormones and growth factors interact with the hemocytoblasts (hemocytoblasts have special receptors on their plasma membranes) that cause a specific pathway of blood cell differentiation
o RBC formation is caused by hormone erythropoietin (EPO)
o The formation of new blood cells occur in blood sinusoids (large, wide blood vessels found in bone marrow) and eventually are released into the blood stream.

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14
Q

Erythropoiesis:

A

o Erythropoiesis = red blood cell production
o A hemocytoblast (or stem cell) differentiates into a proerythroblast (has a nucleus and organelles)
o Proerythroblasts develop into early erythroblasts which produce lots of ribosomes (manufactures protein)
o Hb is synthesized by ribosomes along with the insertion of iron—–the new cell type that is formed is called a late erythroblast
o Late erythroblast becomes a normoblast
o Normoblasts ejects the nucleus and organelles to form reticulocytes (ribosomes is still present to manufacture lots of Hb)
o Reticulocytes then become a biconcave cell
o Reticulocytes then become mature erythrocytes after ribosomes are completely broken down and removed
o Reticulocytes make up 1-2% of all erythrocytes: Recticulocyte Count (retic count)= a blood test that measures how fast reticulocytes are being made by the bone marrow. (usually 1-2 days)
o For Example: a higher reticulocyte count might be indicative of anemia (not enough RBCs) and used as a quick way to check if the anemia is being resolved.

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15
Q

Regulation of Erythropoiesis:

A

o Too few RBCs leads to tissue hypoxia
o Too many RBCs increases blood viscosity
o Balance between RBC production and destruction depends on:
o Hormonal controls
o Adequate supplies of iron, amino acids, and B-12

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16
Q

Hormonal Control of Erythropoiesis:

A
o	Erythropoietin (EPO) = Hormone responsible for stimulus for erythropoiesis (RBC formation) à Produced and released by the kidneys (renal cortex) in response to hypoxia 
o	HIF (hypoxic-inducible factor) = it accumulates in kidney cells when oxygen levels have decreased which triggers production and release of EPO in the kidneys
o	Effects of Erythropoietin =More rapid maturation of committed bone marrow cells through hematopoiesis. Increased circulating reticulocyte count in 1–2 days
o	Testosterone: also enhances EPO production, resulting in higher RBC counts in males
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17
Q

Causes of Hypoxia:

A

o Hemorrhage or increased RBC destruction reduces RBC numbers
o Insufficient hemoglobin (e.g., iron deficiency)
o Reduced availability of O2 (e.g., high altitudes) = altitude sickness (above 8,000 ft.)

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18
Q

Homeostasis of Normal Blood Oxygen Levels:

A

o 1) Hypoxia occurs: Low blood oxygen carrying ability due to: decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2.
o 2) Kidney (and liver to a smaller extent): release erythropoietin.
o 3) Erythropoietin stimulates red bone marrow.
o 4) Enhanced erythropoiesis increases RBC count.
o 5) O2 carrying ability of blood increases.

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19
Q

Dietary Requirements for Erythropoiesis:

A

o Nutrients—amino acids, lipids, vitamins, and carbohydrates
o Iron: Stored in Hemoglobin (= 65%), the rest in the liver, spleen, and bone marrow
o Since free iron is toxic, it is stored in cells as ferritin and hemosiderin (proteins that hold and store iron in cells)
o In blood it is transported loosely bound to the protein transferrin to developing erythrocytes for Hb formation
o Vitamin B12 and folic acid (B9)—necessary for DNA synthesis for cell division of the hematocytoblasts (2 million erythocytes per second are made)!

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20
Q

Fate and Destruction of Erythrocytes:

A

o Life span: 100–120 days
o Old RBCs become fragile, and Hb begins to degenerate
o Loose flexibility, and get stuck in the spleen where macrophages engulf dying RBCs (breakdown also occurs in liver and bone marrow)
o Old and damaged RBCs are broken down by macrophages of the spleen, liver, bone marrow
o Hemoglobin is broken down = Heme + Globin (catabolism)
o Iron is salvaged, stored for reuse as ferritin and hemosiderin (mostly stored within cells of liver….but also spleen and bone marrow )
o Iron is released into blood attached to transferin
o The remaining Heme is degraded to a yellow pigment called bilirubin which binds to albumin and transported to the liver via the blood from the spleen and bone marrow
o Bilirubin is excreted in bile by the liver and stored in the gall bladder bile is then secreted into the small intestine
o Degraded pigment leaves the body in feces as stercobilin (produced by intestinal bacteria)
o Globin is broken down into amino acids (catabolism).

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21
Q

Anemia:

A

o Blood has abnormally low O2 carrying capacity.
o A sign or condition rather than a disease itself.
o Low blood O2 levels cannot support normal metabolism.
o Accompanied by fatigue, paleness, shortness of breath, and chills.

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22
Q

Causes and Types of Anemia:

A

o 1) Insufficient numbers of erythrocytes caused by:
o Hemorrhagic anemia: acute blood loss(trauma) or chronic loss of blood (ulcers)
o Hemolytic anemia: RBCs rupture prematurely(caused by faulty hemoblobin, mismatched blood, bacteria, parasites)
o Aplastic anemia: destruction or inhibition of red bone marrow (due to chemo, radiation, viruses): stem cell transplanting.
o 2) Low hemoglobin content in RBCs caused by:
o Iron-deficiency anemia = most common
o Secondary result of hemorrhagic anemia or Inadequate intake of iron-containing foods or impaired iron absorption
o Erythrocytes with low Hb due to iron-deficiency are called microcytes.
o 3) Abnormal Hemoglobin:
o Thalassemias (of mediterranean ancestry)
o Absent or faulty in alpha or beta globin chain in hemoglobin
o RBCs are become thin, delicate, and deficient in hemoglobin
o If severe, blood transfusions indicated

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23
Q

Pernicious Anemia:

A

o Deficiency of vitamin B12 prevents the proper formation of RBCs (RBCs become large, pale and called macrocytes)
o There is a lack of intrinsic factor in stomach mucosa needed for small intestine absorption of B12
o Autoimmune destruction of “parietal cells” in stomach lining (which produce intrinsic factor)
o Chronic gastritis seen in elderly people which atrophies stomach lining & destroys parietal cells
o Treated by intramuscular injection of B12 or application of Nascobal (nasal lining gel)

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24
Q

Sickle-Cell Anemia:

A

o Results from a change of a single amino acid in the beta-globin molecule which causes abnormal hemoglobin (HbS = sickle hemoglobin): globin beta chains links together in low 02 conditions.
o Causes RBCs to become sickle or crescent shaped in low-oxygen, infection, dehydration situations & stick to capillary walls.
o RBCs rupture easily, blood capillaries blocked, oxygen transport compromised, causing stroke/massive infection.
o Sickle Cell Trait = one defective gene (heterozygous), resistant to malaria (plasmodium parasite from saliva of mosquitoes)
o Sickle Cell Anemia = two defective genes (homozygous)

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25
Q

Definition and Types of Polycythemia:

A

o Excess RBCs that increase blood viscosity (Hct generally >55%). Can result in increased viscosity, increased BP, stroke, embolism, heart failure
o Types:
o Polycythemia vera = bone marrow cancer
o Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases. Athletes train at a higher elevation to increase RBCs
o Blood doping = athletes own RBCs are harvested and re-introduced just before endurance competition = form of secondary polycythemia

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26
Q

Leukocytes (White Blood Cells):

A

o Make up less than 1% of total blood volume.
o Can leave capillaries via “diapedesis” unlike RBCs (circulatory system is the “subway” system to for WBCs to get to areas for inflammatory or immune responses)
o Move through tissue spaces by ameboid motion and positive chemotaxis (follows chemicals released by damaged tissue = “bloodhounds”)
o Leukocytosis = excessive numbers of WBCs = Body speeds up production of WBC count for infection = over 11,000 WBCs/uL (norm is 5,000-10,000)
o Leukopenia = insufficient numbers of WBCs

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27
Q

Functions of Leukocytes:

A
o	Protection: The many types of WBCs provide a mobile army to fight various pathogens, tumor cells, toxins, and parasites. 
o	WBCs provide protection through:
o	Phagocytosis
o	Amplifying the immune response
o	 Specific immune processes
28
Q

Types of Leukocytes and Percentage Make-up:

A
o	Granulocytes: 
     o	Neutrophils: 50-70%
     o	Eosinophils: 2-4%
     o	Basophils: 0.5-1%
o	Agranulocytes:
     o	Lymphocytes: 25-45%
     o	Monocytes: 3-8%
29
Q

Granulocytes:

A

o Neutrophils, eosinophils, and basophils:
o General Characteristics =
o 1) Membrane bound cytoplasmic granules that stain with Wright’s stain
o 2) Larger and shorter-lived than RBCs
o 3) Lobed nuclei
o 4) Phagocytic

30
Q

Neutrophils (50-70%):

A

o Neutrophils are the most numerous of the WBCs (50-70%)
o Also referred as Polymorphonuclear leukocytes (or PMNs), nucleus is multilobed & takes up many shapes, twice the size of RBCs
o Fine cytoplasmic granules take up both acidic and basic dyes
o Cytoplasm takes on a lilac color
o Granules contain antimicrobial hydrolytic enzymes called defensins, which poke holes into microbial membranes (=lysis)
o Very phagocytic—“bacteria slayers” and chemically attracted to debris, dead cells, bacteria (positive chemotaxis)
o 1st WBC to arrive on the scene!!

31
Q

Eosinophils (2-4%):

A

o They are red-staining, bilobed nuclei, and the size of neutrofils
o Red to crimson (acidophilic) coarse, lysosome-like granules.
o Digestive enzymes which destroy parasites
o Eosinophils “inhibit” the release of HISTAMINE from mast cells resulting in the slowing down of inflammation
o Modulators of the immune response: see an increase of eosinophils with allergies, autoimmune diseases, asthma, parasitic infections.

32
Q

Basophils (0.5-1%)

A

o Rarest of the WBCs with bilobed nucleus
o Cytoplasm has large, purplish-black (basophilic) granules which contain histamine / heparin
o Releases histamine = an inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites (amplifies the immune response). Also makes capillaries more permeable.
o Histamine causes smooth muscle constriction of bronchioles
o Releases heparin = an anticoagulant

33
Q

Agranulocytes:

A

Lymphocytes and Monocytes.
o No cytoplasmic granules
o Have spherical or kidney-shaped nuclei

34
Q

Lymphocytes (25%):

A

o Large, dark-purple, circular nuclei that takes up most of the cytoplasm
o Mostly in lymphoid tissue (lymph nodes/spleen); very few circulate in the blood
o Crucial to immunity
o Two types:
o T lymphocytes act against virus-infected cells and tumor cells (they work within cells for intracellular defense = cellular immunity)
o B lymphocytes give rise to plasma cells which produce antibodies (immunoglobins) that work outside cells (extracellular) for body defense

35
Q

Monocytes (3-8%):

A

o The largest of the leukocytes
o Abundant pale-blue cytoplasm
o U- or kidney-bean shaped nuclei
o Monocytes leave circulation, enter tissues, and differentiate into macrophages
o They are actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections (tuberculosis)
o Also activates the immune response and causes the formation of more lymphocytes

36
Q

Leukopoiesis:

A

o Leukopoiesis is the production of WBCs
o It is stimulated by chemical messengers (glycoproteins) from bone marrow and mature WBCs
o Interleukins (are cytokines = chemical messengers) from other cells stimulate the differentiation of hemocytoblasts to leukocytes (can increase or decrease an immune response) examples are EPO, thrombopoietin.
o Colony-stimulating factors (CSFs) = are chemical messengers named for the “WBC type” they stimulate (e.g., granulocyte-CSF stimulates formation of granulocytes from hemocytoblast). Found in certain cells lining blood vessels
o All leukocytes originate from hemocytoblasts.

37
Q

Leukocyte Disorders:

A

o Leukopenia: Abnormally low WBC count—drug induced (anticancer drugs) or radiation treatments. Also caused by immunosuppresent drugs.
o Leukocytosis = high WBC count caused by leukemias or infections
o Leukemias = are cancerous conditions involving WBCs
o Leukemias = are named according to the abnormal leukocyte stem cells involved: formation of unspecialized myeloblasts (stem cells which become granulocytes) and lymphoblasts (stem cells that become lymphocytes) where cell division is out of control and hence produces defective leukocytes that cannot protect
o Myelocytic leukemia involves myeloblasts (most common in adults)
o Lymphocytic leukemia involves lymphoblasts.

38
Q

Platelets (Thrombocytes):

A

o Platelets are not whole cells but small cytoplasmic fragments of megakaryocytes (hemocytoblast is the stem cell)
o Formation is regulated by thrombopoietin
o Blue-staining outer region, purple granules

39
Q

Hemostasis:

A

o 1) Vascular spasm (vasoconstriction)
o 2) Platelet plug formation
o 3) Coagulation (blood clot formation)

40
Q

Platelet Functions:

A

o Secretes PDGF (platelet derived growth hormone) stimulates mitosis of fibroblasts and smooth muscle that help repair vascular wall)
o Secretes vasoconstrictors (e.g. serotonin, thromboxane A2) that causes vascular spasms in broken blood vessels
o Form platelet plugs that stop bleeding (ADP)
o Secrete chemicals that attract neutrophils and monocytes to damaged area (chemotaxis) to clean things up
o HEMOSTASIS = sequence of events that stops bleeding.

41
Q

Step 1 of Hemostasis:

Vascular Spasm

A

Reduction of Blood Loss
o The contraction of smooth muscle of the blood vessel as a response to blood vessel damage and bleeding.
o Reduces blood loss for 20 to 30 minutes, allowing time for clotting to occur.
o Occurs by release of chemicals by platelets and by endothelial cells (serotonin and thromboxane A2) that line the blood vessels & damaged smooth muscle of blood vessels.

42
Q

Step 2 of Hemostasis:

Platelet Plug Formation

A

o A positive feedback cycle
o At the site of blood vessel injury:
o 1) Platelets stick to exposed collagen molecules on damaged endothelial wall of blood vessels
o 2) Platelets swell, become spiked and sticky, and release chemical messengers from their cytoplasmic granules:
o ADP causes more platelets to aggregate and stick together
o Serotonin and thromboxane A2 (vasocontrictors) enhance vascular spasm and more platelet aggregation
o More and more platelets stick together to form a plate plug

43
Q

Step 3 of Hemostasis:

Coagulation

A

o Coagulation involves a set of enzymatic reactions.
o Blood is transformed from a liquid to a gel (clot) through the formation of fibrin (like a spider web).
o Fibrin comes from the plasma protein fibrinogen.
o Involves thirteen known Clotting Factors specified by Roman Numerals if a particular factor(s) are missing or defective = hemophilia.
o A blood clot = insoluble protein fibers (fibrin) and the formed elements that become trapped within the fibrin spider web.

44
Q

The 4 Phases of Coagulation:

A

o Phase 1: Prothrombin activator (or Prothrombinase) is an enzyme formed through both intrinsic and extrinsic pathways.
o Phase 2: Prothrombinase (enzyme) converts prothrombin (plasma protein made in the liver) to thrombin ( an enzyme).
o Phase 3: Thrombin catalyzes fibrinogen (remember…one of the plasma proteins) to form an insoluble fibrin protein (like strands or filaments).
o Phase 4: Fibrin protein clumps together to form a fibrin mesh which “catches” erythrocytes and platelets like a spiderweb.

45
Q

Phase 1 of Coagulation:

A

o Initiated by either the intrinsic or extrinsic pathway; both pathways interact.
o Both triggered by tissue-damaging events. Both pathways lead to formation of prothrombinase (also called prothrombin activator).
o Intrinsic pathway:
o Is triggered by negatively charged surfaces (damaged platelets, exposed collagen)
o Occurs from the rupture of the endothelium lining the blood vessels
o Coagulation occurs over a longer period of time (several minutes)
o Uses factors present within the blood (intrinsic)
o Extrinsic pathway
o Is triggered by exposure to tissue factor (TF) or thromboplastin (Factor III).
o These factors come from the surface of damaged cells after tissue trauma.
o Bypasses several steps compared to the intrinsic pathway-so it is very fast (15 secs).

46
Q

Phase 2 of Coagulation:

A

o Final Result = “Prothrombinase” (enzyme) catalyzes the transformation of prothrombin to the active enzyme thrombin.
o End result for both intrinsic and extrinsic pathways toward the formation of fibrin.

47
Q

Phase 3 of Coagulation:

A
o	Thrombin (an enzyme) = converts soluble fibrinogen into insoluble fibrin.
o	Fibrin strands form the structural basis of a clot.
48
Q

Phase 4 of Coagulation:

A
o	Fibrin causes plasma to become a gel-like “spider web” trap for platlets and RBCs.
o	Thrombin (with Ca2+) activates factor XIII which causes the cross-linking of fibrin, and Strengthens and stabilizes the clot.
49
Q

Clot Retraction:

A

o Actin and myosin (contractile proteins) are in platelets (of the platelet plug) and contract within 30–60 minutes
o Platelets pull on the fibrin strands:edges of damaged vessels are pulled closer together and serum is squeezed from the clot.

50
Q

Clot Repair:

A

o Platelets release Platelet-derived growth factor (PDGF) which stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall.
o Platelets also release Vascular endothelial growth factor (VEGF) which stimulates endothelial cells to multiply and restore the endothelial lining.

51
Q

Fibrinolysis (Clot Breakdown):

A
o	Begins within two days after clot formation.
o	Plasminogen (plasma protein made in the liver) lodges in the clot and is converted to plasmin (enzyme) by tissue plasminogen activator (tPA) (found in endothelial cells lining the blood vessels)
o	There is a genetically engineered drug to treat heart attacks and strokes that breaks blood clots down = tissue plasminogen activator (t-PA)
o	Plasmin (enzyme) breaks down fibrin clot
52
Q

Factors Limiting Clot Growth or Formation:

A

o Two homeostatic mechanisms prevent clots from becoming large (positive feedback mechanism needs to be stopped!!) =
o 1) Swift removal and dilution of clotting factors
o 2) Inhibition of activated clotting factors

53
Q

Inhibition of Clotting Factors:

A

o Most thrombin is bound to fibrin threads, and prevented from acting elsewhere.
o Thrombin not bound to fibrin threads is inactivated by Antithrombin III (plasma protein), protein C (plasma protein produced in liver), and heparin.
o Heparin is a natural anticoagulant found in mast cells and inhibits thrombin.

54
Q

Factors Preventing Undesirable Clotting:

A

o Platelet adhesion is prevented by: Smooth endothelial lining of blood vessels (High BP and infection damages walls, along with atherosclerosis).
o Endothelial cells secrete Antithrombic substances nitric oxide and prostacyclin which act like “teflon” on BV walls
o Vitamin E which acts as a possible anticoagulant

55
Q

Disorders of Hemostasis:

A

o 1) Thromboembolytic disorders = undesirable clot formation.
o 2) Bleeding disorders = abnormalities that prevent normal clot formation.

56
Q

Thromboemolytic Conditions:

A

o Thrombus: a blood clot that develops and persists in an unbroken blood vessel (most likely in a vein) or heart chamber (pooling of blood) and can be related to blood stagnation or pooling (due to inactivity), atrial fibrillation, genetics or disease state which interferes with blood clotting.
o May block circulation, leading to tissue death.
o Embolus: a thrombus that has dislodged and freely floats in the blood stream.
o Pulmonary emboli (lung) impairs the body to obtain oxygen.
o Cerebral emboli (brain) can cause strokes (CVA).
o Coronary emboli (heart) causes a MI .
o Coagulation prevented by:
o Aspirin. An antiprostaglandin that blocks synthesis of thromboxane A2 (a prostaglandin produced by platelets). Blocks platelet aggregation and vascular spasm
o Heparin: An anticoagulant used clinically for pre- and postoperative cardiac care (works against thrombin formation)
o Warfarin (Coumadin): Used to prevent stroke for those prone to atrial fibrillation (causes blood to pool in heart). Interferes with action of vitamin K (needed for clotting factors).

57
Q

Bleeding Disorders:

Thrombocytopenia

A

o Deficient number of circulating platelets.
o Petechiae appear due to spontaneous, widespread hemorrhage. Due to suppression or destruction of bone marrow (e.g., malignancy, radiation).
o Platelet count

58
Q

Bleeding Disorders:

Hemophilias

A

o Hemophilias include several similar hereditary bleeding disorders.
o Hemophilia A: most common type (77% of all cases); due to a deficiency of factor VIII (causing cross linking of fibrin) .
o Hemophilia B: deficiency of factor IX (thromboplastin).
o Hemophilia C: mild type; deficiency of factor XI.
o Symptoms include prolonged bleeding, especially into joint cavities.
o Treated with plasma transfusions and injection of missing factors.

59
Q

Transfusions:

A

o Whole-blood transfusions are used when blood loss is acute or high volume losses greater than 30% can cause severe shock (1.5 liters or about 6 cups).
o Transfusion can also be packed red cells (plasma removed) to restore oxygen-carrying capacity quickly.
o Donated blood lasts about 35 days.

60
Q

Blood Types:

A

o RBC cell surfaces contain glycoproteins called antigens = agglutinogens:
o = Type A blood has Antigen A
o = Type B blood has Antigen B
o = Type AB has both Antigen A & B = universal recipient
o = Type O blood has neither Antigen A or B = universal donor
o Blood plasma contains antibodies = agglutinins to specific antigens (called anti-A and/or anti-B).
o There are over 100 different blood groups (e.g., Rh blood group, MNS, Duffy, Kell, etc.).

61
Q

Blood Typing:

A

o When serum containing anti-A or anti-B agglutinins (antibodies) is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens (antigens on the plasma membrane).
o Positive reactions indicate agglutination.

62
Q

Rh Factor:

A

o Rh+ means you have the Rh antigen on the surface of your RBCs.
o Rh- means you don’t have the Rh antigen on the surface of your RBCs.
o 85% of whites, 88% of blacks, 99% of Asians are Rh+.
o Antibodies against the Rh antigen DO NOT DEVELOP unless an Rh negative person is exposed to Rh positive blood, after exposure, antibodies will then develop against the Rh antigen.
o Rh- person can give to Rh- and Rh+ individuals.
o Rh+ person can only give to Rh+, not a Rh- individual (will lead to anti Rh+ antibodies which can cause erythroblastosis fetalis in later years for pregnant women).

63
Q

HDN (Hemolytic Dz of Newborn):

A

o Scenario: Rh (-) mom has a Rh (+) baby.
o Usually not a problem in the first pregnancy.
o In the 2nd pregnancy, the mom has produced anti-Rh antibodies from the 1st pregnancy which can cross the placenta if there is a blood to blood exposure due to a tear in the placenta.
o > The anti-Rh antibodies attack the RBCs of the fetus and causes hemolysis of RBCs (erythroblastosis fetalis).
o Can be prevented with RhoGAM injection at time of first birth = binds baby’s Rh factor and blocks immune response from mom.

64
Q

Transfusion Reactions:

A

o War between the patient’s own blood and the blood that is being transfused
o Can cause clumping (agglutination) and resulting hemolysis of red blood cell hemoglobin (iron) is released into plasma which is BAD, could lead to.
o Anemia, fever, chills, low BP
o Kidney damage (Hb damages nephron tubules)
o Clog small blood vessels on lungs, heart, brain, kidneys (ULTIMATE DEATH).

65
Q

Restoring Blood Volume:

A

o Death from shock may result from low blood volume
o Volume must be replaced immediately with
o Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition.
o Plasma expanders (e.g., purified human serum albumin). Mimic osmotic properties of albumin (water follows solutes, hence more water in blood). More expensive and may cause significant complications.