Physiology of Blood

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blood clot/gas bubble floating in blood: embolus
factors interfere with normal clotting: 1. prothrombin III - deactivates thrombin
2. protein C - inhibits clotting Factors
3. heparin - inhibits thrombin; prevents adherence of platelets to injured site
undesirable clotting: Thromboembolytic Disorders
blood clot in normal blood vessel: thrombus
can dissolve a clot: TPA, streptokinase
inhibits Thromboxane formation: aspirin
inhibits thrombin & platelet deposit: heparin
anticoagulant, blocks Vitamin K: dicumarol
reduced platelet count; generally below 50,000 per cubic millimeter; can cause excessive bleeding from vascular injury: thrombocytopenia
impaired liver function - lack of (Clotting Factors) that are made in liver: procoagulants
essential for liver to make Clotting Factors for coagulation: vitamin K
hereditary bleeding disorders that occur almost exclusively in males: hemophilias
hemophilias defective Factor VIII (83%): hemophilia A
hemophilias defective Factor IX (10%): hemophilia B
hemophilias now produces genetically engineered TPA and Factor VIII; patients do not need transfusions as often: Genentech. Inc.
all cells and plasma; anticoagulants (citrate and oxalate salts) used: whole blood transfusion
most of the plasma has been removed prior to transfusion: packed red blood cells
glycoproteins on the surface of blood cells; causes "agglutination" (clumping): agglutinogens
determined by presence or absence of Type A and Type B agglutinogen proteins on cell membrane: ABO Blood Groups
NO Rh factor: Rh negative (Rh-)
an Rh factor is present: Rh positive (Rh+)
type A blood: GENES: A/A, A/O, O/A
PEOPLE: (30-40%)
Antibodies: Anti-B
Receive Blood from: A, O
type B blood: GENES: B/B, B/O, O/B PEOPLE: (l0-30%)
Antibodies: Anti-A
Receive Blood from: B,O
type AB blood: GENES: A/B or B/A PEOPLE: (3-5%)
Antibodies: none
Receive Blood from: A, B, AB, O
type O blood: GENES: no A or B PEOPLE: (40-50%)
Antibodies: Anti-A, Anti-B
Receive Blood from: O only
Diagnostic Blood Tests blood glucose level: diabetes
antibodies against either A or B agglutinogen (whichever is not present) a. transfusion reaction - patient's antibodies attack the donor blood: agglutinins
transfusion reaction - patient's antibodies attack the donor blood: A (anti-B) receives A,O (not B)
B (anti-A) receives B,O (not A)
AB (none) receives A, B,AB,O (universal recipient)
O (anti-A,anti-B) receives O
(universal donor)
antibodies against either A or B agglutinogen (whichever is not present): agglutinins
when incorrect blood transfused, antibodies will "clump" new blood: agglutination
after clumping, RBCs may rupture, releasing hemoglobin, harming kidney: hemolysis
hemolysis, treatment for:: dilute hemoglobin, administer diuretics
a different group of agglutinogens: Rh factor
delayed and less severe than in ABO confrontation: transfusion reaction
directly from the mother (Rh-) to the newborn (Rh+): exchange transfusion
Rh- mother antibodies attack Rh+ of older newborn; results in anemia and low oxygen levels (hypoxia): erythroblastosis fetalis
Diagnostic Blood Tests lipidemia: high in fat; yellowish plasma
serum with anti-Rh agglutinins which will clump the Rh factor, blocking the reaction of motherÂ’s antibodies: RhoGAM
mixing Donors Blood with Recipient Antibodies (Anti-A, Anti-B, anti-Rh) in order to identify agglutination: Blood Typing
Diagnostic Blood Tests generally higher WBC count: infection
Diagnostic Blood Tests significantly higher WBC count: leukemia
Ways of Expanding Blood Volume to Avoid Shock: 1. pure plasma without antibodies
2. plasma expanders - purified human serum albumin, plasminate, dextran
3. isotonic saline - normal electrolyte solution isotonic to blood plasma (Ringer's Solution)
Diagnostic Blood Tests anemia: low hematocrit (below 35%)
Diagnostic Blood Tests counts % of each of the different leukocytes (helps diagnose): differential WBC count
Diagnostic Blood Tests time for clotting to occur: prothrombin time
Diagnostic Blood Tests diagnose thrombocytopenia: platelet count
Diagnostic Blood Tests overall blood review: complete blood count
Factors Limiting Growth and Formation of Clots Limiting Normal Clot Growth: a. blood moves too fast to allow procoagulants
b. factors interfere with normal clotting
Clot Eradication (Fibrinolysis) healing occurs over ? days: healing occurs over 2 - 10 days
Clot Eradication (Fibrinolysis) causes the activation of plasminogen: tissue plasminogen activator (TPA)
Clot Eradication (Fibrinolysis) plasminogen--> ?: plasmin
Clot Eradication (Fibrinolysis) ? degrades proteins within the clot: plasmin
the actual cellular components of blood (special connective tissue): formed elements

erythrocytes
leukocytes
platelets
complex non-cellular fluid surrounding formed elements; protein & electrolytes: blood plasma
Separation of Components in a Centrifuge VOLUME LAYER 55% top: clear/yellowish PLASMA
Separation of Components in a Centrifuge VOLUME LAYER <1% middle: thin/whitish buffy coat
with LEUKOCYTES & PLATELETS
Separation of Components in a Centrifuge VOLUME LAYER 45% bottom: reddish mass - ERYTHROCYTES
red blood cells: erythrocytes
white blood cells: leukocytes
cell fragments for clotting: platelets
percentage by VOLUME of erythrocytes when blood is centrifuged (normal = 45%): hematocrit
Characteristics of Blood bright red: oxygenated
Characteristics of Blood dark red/purplish: unoxygenated
Characteristics of Blood: 1. much more dense than pure water
2. pH range from 7.35 to 7.45 (slightly alkaline)
3. slightly warmer than body temperature 100.4 F
4. typical volume in adult male 5-6 liters
5. typical volume in adult female 4-5 liters
6. typically 8% of body weight
Distribution & Transport: a. oxygen from lungs to body cells
b. carbon dioxide from body cells to lungs
c. nutrients from GI tract to body cells
d. nitrogenous wastes from body cells to kidneys
Regulation (maintenance of homeostasis) maintenance of normal body pH: blood proteins (albumin) & bicarbonate
Regulation (maintenance of homeostasis) maintenance of circulatory/interstitial fluid: electrolytes aid blood proteins (albumin)
Regulation (maintenance of homeostasis): maintenance of temperature (blushed skin)
Protection "seal" vessel damage: platelets and proteins
Protection leukocytes, antibodies, complement proteins: protection from foreign material & infections
Erythrocytes (red blood ells; RBCs) Structure diameter / thickness: 7.5 micron diameter; 2.0 micron thick
Erythrocytes (red blood ells; RBCs) Structure ideal for gas exchange: biconcave disk shape
Erythrocytes (red blood ells; RBCs) Structure elastic protein; allows shape change: spectrin
Erythrocytes (red blood ells; RBCs) Structure anucleate (no nucleus): mature cells
Erythrocytes (red blood ells; RBCs) Structure very few organelles; mainly a hemoglobin carrier: hemoglobin Â– 33% of cell mass; carries oxygen
Erythrocytes (red blood ells; RBCs) Structure only anaerobic respiration: no mitochondria
Erythrocytes (red blood ells; RBCs) Structure ratio erythrocytes:leukocytes: 800:1
Erythrocytes (red blood ells; RBCs) Structure red blood cell count: # cells per cubic millimeter i. normal male count: 5.1 to 5.8 million
Erythrocytes (red blood ells; RBCs) Structure red blood cell count: # cells per cubic millimeter i. normal female count: 4.3 to 5.2 million
large molecules with globin and hemes: hemoglobin
complex protein with 4 polypeptides (2 alpha and 2 beta polypeptides): globin
IRON containing pigment part of hemoglobin to which oxygen binds: heme group
each polypeptide has: one heme group
each heme carries: one O2
normal hemoglobin levels (grams/l00 ml blood) infants: 14-20 grams/l00 ml
normal hemoglobin levels (grams/l00 ml blood) adult female: 12-16 grams/100 ml
normal hemoglobin levels (grams/l00 ml blood) adult male: 13-18 grams/l00 ml
when oxygen is bound to IRON: oxyhemoglobin
no oxygen bound to IRON: deoxyhemoglobin
when carbon dioxide bound (to polypeptide chain): carbaminohemoglobin
the maturation, development and formation of blood cells: hematopoiesis (hemopoiesis)
location of hematopoiesis; in blood sinusoids which connect with capillaries; mainly in axial skeleton and heads of femur & humerous: red bone marrow (myeloid tissue)
the mitotic precursor to blood cells before differentiation: hemocytoblast (stem cell)
maturing cell becomes "committed" to being certain type blood cell: differentiation
the maturation, development, and formation of Red Blood Cells (erythrocytes): erythropoiesis
erythropoiesis: hemocytoblast ->
proerythroblast ->
early (basophilic) erythroblast ->
late (polychromatophilic) erythroblast->
(hemoglobin) normoblast ->
(nucleus ejected when enough hemoglobin)
reticulocyte ->
(retaining some endoplasmic reticulum)
ERYTHROCYTE
3-5 DAYS: hemocytoblast -> reticulocyte
2 DAYS (in blood): reticulocyte -> ERYTHROCYTE
100-120 DAYS: ERYTHROCYTE lifespan
ERYTHROCYTE death: (primarily destroyed by macrophages in the spleen)
Regulation of Erythropoiesis hormonal controls hormone that stimulates RBC production: erythropoietin
Regulation of Erythropoiesis hormonal controls DECREASED oxygen level in blood causes: KIDNEYS to increase release of erythropoietin
DECREASED oxygen level in blood causes: 1. Less RBCs from bleeding
2. Less RBCs from excess RBC destruction
3. Low oxygen levels (high altitude, illness)
4. Increased oxygen demand (exercise)
Eythropoietin now genetically engineered and synthesized by: AMGEN of Thousand Oaks
Testosterone can also mildly stimulate production of: RBCs in humans
essential for hemoglobin to carry oxygen: Iron
65% of Fe in body is in: hemoglobin
liver and spleen store most excess Fe bound to: ferritin and hemosiderin
Fe in blood bound to: transferrin
daily Fe loss:: 0.9 mg men/l.7 mg women
women also lose Fe during: menstrual flow
essential for DNA synthesis in early mitotic divisions leading to erythrocytes: B-complex Vitamins - Vitamin B12 and Folic Acid
a symptom that results when blood has lower than normal ability to carry oxygen: Anemias
loss of blood from bleeding (wound, ulcer, etc.): hemorrhagic anemia
erythrocytes rupture (hemoglobin/transfusion problems, infection): hemolytic anemia
red marrow problems (cancer treatment, marrow disease, etc.): aplastic anemia
Decrease in Hemoglobin low Iron levels (diet; absorption, bleeding, etc.): iron-deficiency anemia
Decrease in Hemoglobin low Vitamin B12 (diet, intrinsic factor for Vit B absorption): pernicious anemia
Abnormal Hemoglobin (usually genetic) easily ruptured RBCs (Greek & Italian genetic link): thalassemia
Abnormal Hemoglobin (usually genetic) sickle-shaped RBCs (genetic Africa, Asia, southem Europe link): sickle-cell anemia
excess RBC count, causes thick blood: Polycythemia
bone marrow problem; hematocrit may jump to 80%: polycythemia vera
high altitude (normal); or too much erythropoietin release: secondary polycythemia
RBCs previously withdrawn are transfused before an event; more RBCs, more oxygen delivery to the body: blood doping in athletes
Leukocytes (white blood cells; WBCs) General Structure and Function protection from: microbes, parasites, toxins, cancer
Leukocytes (white blood cells; WBCs) General Structure and Function ?% of blood volume; ? per cubic mm blood: 1% of blood volume; 4-11,000 per cubic mm blood
Leukocytes (white blood cells; WBCs) General Structure and Function can "slip between" capillary wall: diapedesis
Leukocytes (white blood cells; WBCs) General Structure and Function movement through the body: amoeboid motion
Leukocytes (white blood cells; WBCs) General Structure and Function moving in direction of a chemical: chemotaxis
Leukocytes (white blood cells; WBCs) General Structure and Function increased "white blood cell count" in response to bacterial/viral infection: leukocytosis
Leukocytes (white blood cells; WBCs) General Structure and Function contain membrane-bound granules (neutrophils, eosinophils, basophils): granulocytes
Leukocytes (white blood cells; WBCs) General Structure and Function NO membrane-bound granules (lymphocytes, monocytes): agranulocytes
granules in cytoplasm can be stained with Wright's Stain; bilobar nuclei; 10-14 micron diameter; all are phagocytic cells (engulf material): Granulocytes
destroy and ingest bacteria & fungi (polymorphonuclear leuks.; "polys"): neutrophils
a. most numerous WBC b. basophilic (blue) & acidophilic (red) c. defensins - antibiotic-like proteins (granules) d. polymorphonuclear - many-lobed nuclei e. causes lysis of infecting bacteria/fungi f. HIGH poly count -->: neutrophils
lead attack against parasitic worms: eosinophils
a. only 1-4% of all leukocytes b. two-lobed, purplish nucleus c. acidophilic (red) granules with digest enzymes d. phagocytose antigens & antigen / antibody complex e. inactivate chemicals released during allergies: eosinophils
releases Histamine which causes inflammation, vasodilation, attraction of WBCs: basophils
a. RAREST of all leukocytes (0.5%) b. deep purple U or S shaped nucleus c. basophilic (blue) granules with HISTAMINE d. related to "mast cells" of connective tissue e. BOTH release Histamine with "IgE" signal: basophils
WBCs without granules in cytoplasm: C. Agranulocytes
(thymus) respond against virus infected cells and tumor cells: T lymphocytes
(bone) differentiate into different "plasma cells" which each produce antibodies against different antigens: B lymphocytes
lymphocytes primarily in: lymphoid tissues
lymphocytes nucleus: very large basophilic (purple) nucleus
small lymphocytes in blood ? microns: 5-8 microns
larger lymphocytes in lymph organs ? microns: 10-17 microns
differentiate to become macrophages; serious appetites for infectious microbes: monocytes
largest of all lymphocytes (18 microns) dark purple, kidney shaped nucleus: monocytes
the production, differentiation, and development of white blood cells: leukopoiesis
hematopoietic hormones that promote leukopoiesis: colony stimulating factors (CSF)
M-CSF: macrophage-monocyte CSF
(colony stimulating factors)
G-CSF: granulocyte CSF
GM-CSF: granulocyte-macrophage CSF
multi CSF: multiple lymphocyte action
IL-3: interleukin 3 (general lymphocytes)
all cells derived from hemocytoblast: leukopoiesis
EOSINOPHIL NEUTROPHIL BASOPHIL lifespan?: 0.5 to 9 day lifespan
abnormally low WBC count: leukopenia
leukopenia causes: HIV infection, glucocorticoids, chemotherapy
cancerous condition of "line" of WBCs: leukemia
myelocytic leukemia: myelocytes
lymphocytic leukemia: lymphocytes
acute leukemia: cancer spreads rapidly
chronic leukemia: cancer progresses slowly
caused by Epstein-Barr virus, excessive monocytes and lymphocytes; fatigue, sore throat, fever; 3 week course: infectious mononucleosis
thrombocytes - "clotting": Platelets
Platelets (thrombocytes - "clotting") size?: very small, 2-4 microns in diameter
Platelets (thrombocytes - "clotting") approximately ? per cubic millimeter: approximately 250-500,000 per cubic millimeter
Platelets (thrombocytes - "clotting") essential for ? of damaged vasculature: essential for clotting of damaged vasculature
regulates platelet production: thrombopoietin
hemocytoblast-> myeloid stem cell-> megakaryoblast-> promegakaryocyte-> megakaryocyte-> (large multilobed nucleus) platelets (anucleated parts of megakaryocyte cytoplasm): Formation of Platelets
plasma makes up ?% of normal blood by volume: plasma makes up 55% of normal blood by volume
water is ?% of the plasma by volume: water is 90% of the plasma by volume
different SOLUTES in the plasma: albumin
globulins
clotting proteins
other proteins
nutrients
electrolytes
pH buffer & osmotic pressure: albumin
binding proteins & antibodies: globulins
clotting proteins: prothrombin & fibrinogen
other proteins: enzymes, hormones, others
glucose, fatty acids, amino acids, cholesterol, vitamins: nutrients
Na+, K+, Ca++, Mg++, Cl-, phosphate, sulfate, bicarbonate, others: electrolytes
stoppage of blood flow after damage: Hemostasis
Hemostasis General Characteristics: 1. vascular spasms (vasoconstriction at injured site)
2. platelet plug formation (plugging the hole)
3. coagulation (blood clotting - complex mechanism)
first response to vascular injury: Vascular Spasms / VASOCONSTRICTION
VASOCONSTRICTION is stimulated by:: a. compression of vessel by escaping blood
b. injury "chemicals" released by injured cells
c. reflexes from adjacent pain receptors
Formation of a Platelet Plug: 1. damage to endothelium of vessel
2. platelets become spiky and sticky in response
3. platelets attach to damaged vessel wall to plug it
4. platelets produce thromboxane A2 - granule release
5. serotonin release enhances vascular spasm
6. ADP - attracts and stimulates platelets at site
7. prostacylin - inhibits aggregation at other sites
Coagulation: blood clotting
General Events in Clotting: platelet cells activated by damage->
PF3 and/or Tissue Factor produced by platelet cells->
Factor X activated->
prothrombin activator (enzyme)produced->
prothrombin conversion -> thrombin (another enzyme)
thrombin stimulates: fibrinogen----> fibrin mesh
chemical that inhibits clotting: anticoagulant
chemical that promotes clotting: procoagulant
pathway - within the damaged vessel: intrinsic pathway
a. more procoagulants needed (I-XIII) toward PF3 and Factor X b. allows more "scrutiny" before clotting occurs: intrinsic pathway
pathway in outer tissues around vessel: extrinsic pathway
skips intrinsic steps straight to PF3 and Factor X: tissue thromboplastin (Tissue Factor)
a. tissue thromboplastin (Tissue Factor) - skips intrinsic steps straight to PF3 and Fac X b. allows rapid response to bleeding out of vessel (clot can form in 10 to 15 seconds): extrinsic pathway - in outer tissues around vessel
After activation of Factor X, common pathway:: Factor X, PF3 (thromboplastin), Factor V, Ca++ -->
prothrombin activator ->
prothrombin converted ->
thrombin (active enzyme)
thrombin stimulates: fibrinogen -> fibrin (meshwork)
Ca++ & thrombin -> Factor XIII (fibrin stabilizer)
shrinking of clot: Clot Retraction
Clot Retraction (shrinking of clot) causes contraction of platelets: actomyosin
Clot Retraction (shrinking of clot) plasma WITHOUT clotting Factors: blood serum - plasma WITHOUT clotting Factors
Clot Retraction (shrinking of clot) stimulates fibroblast migration and endothelial growth: platelet-derived growth factor (PDGF)
Clot Eradication: Fibrinolysis
1. anemia, fever, weight loss, bone pain 2. death from internal hemorrhage or infection 3. chemotherapy & radiation therapy used to treat: leukemia

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