test 1 (blood, heart, blood vessels)

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functions of the circulatory system

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functions of the circulatory system

-transport: O₂, CO₂, nutrients, wastes, hormones, and stem cells

-protection: inflammation, limit spread of infection, destroy microorganisms and cancer cells, neutralize toxins, and initiate clotting

-regulation: fluid balance, stabilizes pH of ECF, and temp control

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plasma

-matrix of blood (45-50% of BV)

-clear, light yellow fluid

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formed elements

-blood cells and cell fragments

-red blood cells, white blood cells, and platelets

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granulocytes

-neurtophils, eosinophils, basophils

-leave in 8 hours and live 5 days longer

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agranulocytes

lymphocytes & monocytes

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albumins

-smallest and most abundant

-contribute to viscosity and osmolarity

-influence blood pressure, flow, and fluid balance (regulates fluid volume)

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globulins

-antibodies

-provide immune system functions

-alpha, beta, and gamma

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fibrinogen

precursor of fibrin threads that help form blood clots

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nitrogenous compounds

-free amino acids from dietary protein or tissue breakdown

-urea

-toxic end products of catabolism

-normally removed by the kidneys

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viscosity

resistance of a fluid to flow, resulting from the cohesion of its particles

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osmolarity of blood

-the total molarity of those dissolved particles that can’t pass through the blood vessel wall

-if too high, blood absorbs too much water, increasing BP

-if too low, too much water stays in tissue, BP drops, and edema occurs

-optimum level is achieved by the body’s regulation of sodium ions, proteins, and RBCs

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hemopoiesis

production of blood, especially its formed elements

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hemopoietic tissues

-yolk sac produces stem cells for first blood cells

-liver stops producing blood cells at birth

-spleen remains involved with lymphocyte production, more for storage

-mostly made in bone marrow

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colony-forming unit

specialized stem cells only producing one class of formed element of blood

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myeloid hemopoiesis

blood formation in the bone marrow

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lymphoid hemopoiesis

blood formation in the lymphatic organs (beyond infancy this only involves lymphocytes)

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erythrocyte functions

-carry oxygen from lungs to cell tissues

-pick up CO₂ from tissues and bring to lungs

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erythrocyte features

-lack mitochondria; anaerobic fermentation to produce ATP

-lack of nucleus and DNA; no protein synthesis or mitosis

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carbonic anhydrase (CAH) in cytoplasm

-produces carbonic acid from CO₂ & water

-important role is gas transport and pH balance

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hemoglobin features

-adult has 2 alpha and 2 beta chains

-fetal contains 2 alpha and 2 gamma chains

-4 heme groups

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heme groups

nonprotein moiety that binds O₂ to ferrous iron (Fe) at its center

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hematocrit

-packed cell volume

-percentage of whole blood volume composed of RBCs

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erythrocyte production

-average lifespans=about 120 days

-development takes 3-5 days

-first committed cell= erythrocyte colony-forming unit that has receptors for erythropoietin (EPO) from kidneys

-erythroblasts multiply and synthesize hemoglobin

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liver apoferritin

-binds to create ferritin for storage of Fe

-reduction of free iron reduces bacterial growth in blood plasma

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negative feedback control (erythrocytes)

-drop in RBC count causes hypoxemia detected by kidney

-kidney production of erythropoietin stimulates bone marrow

-RBC count increases in 3-4 days

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stimuli for increasing erythropoiesis

-low levels O₂ (hypoxemia)

-high altitude

-increase in exercise

-loss of lung tissue in emphysema

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erythrocyte death & disposal

-RBCs rupture (hemolysis) in narrow channels of spleen and liver

-macrophages in spleen; digest membrane bits; separate heme from globin

-globins hydrolyzed into amino acids

-iron removed from heme

-heme pigment converted to biliverdin (green); biliverdin converted to bilirubin (yellow); released into blood plasma (kidneys- yellow urine); liver removes bilirubin and secretes into bile; concentrated in gallbladder, released into small intestine, bacteria create urobilinogen (brown)

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polycythemia

excess of RBCs

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primary polycythemia (polycythemia vera)

-cancer of erythropoietic cell line in red bone marrow

-RBC count as high as 11 million RBCs/µL; hematocrit 80%

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secondary polycythemia

-from dehydration, emphysema, high altitude, or physical conditioning

-RBC count up to 8 million RBCs/µL

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dangers of polycythemia

-increased blood volume, pressure, viscosity

-can lead to embolism, stroke, or heart failure

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causes of anemia

-inadequate erythropoiesis or hemoglobin synthesis

-kidney failure and insufficient erythropoietin

-iron deficiency

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pernicious anemia

autoimmune attack of stomach tissue leads to inadequate vitamin B₁₂ absorption

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hypoplastic anemia

slowing of erythropoiesis

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aplastic anemia

complete cessation of erythropoiesis

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hemorrhagic anemia

from bleeding

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hemolytic anemia

from RBC destruction

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anemia consequences

-tissue hypoxia and necrosis (patient is lethargic; shortness of breath upon exertion; life-threatening necrosis of brain , heart, or kidney)

-blood osmolarity is reduced, producing tissue edema

-blood viscosity is low (heart races and pressure drops; cardiac failure may ensue)

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antigens

-complex molecules on surface of cell membrane that activate an immune response

-genetically unique to the individual

-used to distinguish self from foreign matter

-foreign antigens generate an immune response

-A, B, Rh (D)

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agglutinogens

antigens on the surface of the RBC that are the basis for blood typing

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antibodies

-proteins (gamma globulins) secreted by plasma cells

-part of immune response to foreign matter

-bind to antigen and mark them for destruction

-forms antigen-antibody complexes

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agglutinins

-antibodies in the plasma that bring about transfusion mismatch

-anti-A, anti-B, & anti-Rh

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clumping (agglutination)

-antibody molecule binding to antigens

-causes clumping of RBCs

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universal donor

-type O-

-lack RBC antigens

-donor’s plasma may have both antibodies against recipient’s RBCs (anti-A, anti-B, anti-Rh)

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universal recipient

-type AB+

-lacks plasma antibodies; no anti-A, anti-B, or anti-Rh

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neutrophil

-60-70%

-barely visible granules in cytoplasm; 3-5 lobed nucleus

-aggressively antibacterial

<p>-60-70%</p><p>-barely visible granules in cytoplasm; 3-5 lobed nucleus</p><p>-aggressively antibacterial</p>
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eosinophil

-2-4%

-large rosy-orange granules; bilobed nucleus

-increased numbers in parasitic infections, collagen diseases, allergies, diseases of spleen and CNS

-release enzymes to destroy large parasites

<p>-2-4%</p><p>-large rosy-orange granules; bilobed nucleus</p><p>-increased numbers in parasitic infections, collagen diseases, allergies, diseases of spleen and CNS</p><p>-release enzymes to destroy large parasites</p>
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basophil

-less than 1%

-large abundant, violet granules (obscure S-shaped nucleus)

-increased numbers in chickenpox, sinusitis, diabetes

-secrete histamine & heparin

<p>-less than 1%</p><p>-large abundant, violet granules (obscure S-shaped nucleus)</p><p>-increased numbers in chickenpox, sinusitis, diabetes</p><p>-secrete histamine &amp; heparin</p>
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lymphocyte

-25-33%

-variable amounts of bluish cytoplasm (scanty to abundant); ovoid/round, uniform dark violet nucleus

-increased number in diverse infections and immune responses

-destroy human cells (cancer, foreign, and virally infected cells)

-secrete antibodies and provide immune memory

-provide long-term immunity (decades), being continuously recycled from blood to tissue fluid to lymph and back to the blood

<p>-25-33%</p><p>-variable amounts of bluish cytoplasm (scanty to abundant); ovoid/round, uniform dark violet nucleus</p><p>-increased number in diverse infections and immune responses</p><p>-destroy human cells (cancer, foreign, and virally infected cells)</p><p>-secrete antibodies and provide immune memory</p><p>-provide long-term immunity (decades), being continuously recycled from blood to tissue fluid to lymph and back to the blood</p>
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monocyte

-3-8%

-usually largest WBC; ovoid, kidney, or horseshoe-shaped nucleus

-increased numbers in viral infections and inflammation

-leave in 20 hours, transform into macrophages, and live for several years

<p>-3-8%</p><p>-usually largest WBC; ovoid, kidney, or horseshoe-shaped nucleus</p><p>-increased numbers in viral infections and inflammation</p><p>-leave in 20 hours, transform into macrophages, and live for several years</p>
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histamine

-vasodilator

-speeds flow of blood to an injured area

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heparin

-anticoagulant

-promotes the mobility of other WBCs in the area

-from basophils and mast cells

-interferes with formation of prothrombin activator

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leukopoiesis

production of white blood cells

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hemopoietic stem cells (HSCs) differentiate into

-myeloblasts: form neutrophils, eosinophils, basophils

-monoblasts: form monocytes

-lymphoblasts: form lymphocytes

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hemostasis

-the cessation of bleeding

-stopping potentially fatal leaks

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hemostatic mechanisms

-vascular spasm

-platelet plug formation

-blood clotting (coagulation)

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platelets (thrombocytes)

-small fragments of megakaryocyte cells

-contain a complex internal structure and an open canalicular system

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platelet functions

-secrete vasoconstrictors that help reduce blood loss

-stick together to form platelet plugs to seal small breaks

-secrete procoagulants or clotting factors to promote clotting

-initiate formation of clot-dissolving enzyme

-chemically attract neutrophils and monocytes to site of inflammation

-phagocytize and destroy bacteria

-secrete growth factors that stimulate mitosis to repair blood vessels

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thrombopoiesis

stem cells (that develop receptors for thrombopoietin) become megakaryoblasts

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megakaryoblasts

-repeatedly replicate DNA without diving

-form gigantic cells called megakaryocytes with a multilobed nucleus

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megakaryocytes

-live in bone marrow adjacent to blood sinusoids

-long tendrils of cytoplasm (proplatelets) protrude into the blood sinusoids, blood flow splits off fragments called platelets

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vascular spasm

-prompt constriction of a broken vessel

-most immediate protection against blood loss

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vascular spasm causes

-pain receptors, some directly innervate blood vessels to constrict

-smooth muscle injury

-platelets release serotonin (vasoconstrictor)

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vascular spasm effects

-prompt constriction of a broken vessel

-pain receptors (short duration)

-smooth muscle injury (longer duration)

-provides time for other 2 clotting pathways

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platelet plug formation

-intact vessels have a smooth endothelium coated with prostacyclin (a platelet repellent)

-broken vessels exposes collagen

-platelet pseudopods stick to damaged vessel and other platelets

-pseudopods contract—draw together a platelet plug

-platelets degranulate releasing a variety of substance (serotonin, ADP, etc.)

-positive feedback loop

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coagulation (clotting)

-last and most effective defense against bleeding

-conversion of plasma protein fibrinogen into insoluble fibrin threads to form frame work of clot

-procoagulants (clotting factors)—usually produced by the liver; are present in plasma

-activate one factor and it will activate the next to form a reaction cascade

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extrinsic pathway

-factors released by damaged tissues begin cascade

-2 proteins

-initiated by release of tissue thromboplastin (factor III) from damaged tissue

-cascade to factor VII, V, and X (fewer steps)

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intrinsic pathway

-factors found in blood begin cascade (platelet degranulation)

-4 proteins

-initiated by platelets releasing Hageman factor (factor XII)

-cascade to factor XI to IX to VIII to X

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completion of coagulation

-activation of factor X (leads to production of prothrombin activator)

-prothrombin activator (converts prothrombin to thrombin)

-thrombin (converts fibrinogen into fibrin monomers; monomers covalently bind to form fibrin polymer; factor XIII cross links fibrin polymer strands)

-positive feedback (thrombin speeds up formation of prothrombin activator)

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fibrinolysis

-dissolution of a clot

-factor XII speeds up formation of kallikrein enzyme

-kallikrein converts plasminogen into plasmin, a fibrin-dissolving enzyme that breaks up the clot

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platelet repulsion

platelets do not adhere to prostacyclin-coated endothelium

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thrombin dilution

-by rapidly flowing blood

-heart slowing in shock can result in clot formation

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antithrombin

-from liver

-deactivates thrombin before it can act on fibrinogen

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hemophilia

-family of hereditary diseases characterized by deficiencies of one factor or another

-Sex-linked recessive (on X chromosome)

-Hemophilia A missing factor VIII (83% of cases)

-Hemophilia B missing factor IX (15% of cases)

-Hemophilia C missing factor XI (autosomal)

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hemophilia A

-physical exertion causes bleeding and excruciating pain

-transfusion of plasma or purified clotting factors

-factor VIII produced by transgenic bacteria

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hematomas

masses of clotted blood in the tissues

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thrombosis

abnormal clotting in unbroken vessel

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Thrombus

-clot (stationary)

-most likely to occur in leg veins of inactive people

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pulmonary embolism

clot may break free, travel from veins to lungs

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embolus

anything that can travel in the blood and block blood vessels (moving)

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vitamin K

-is required for formation of clotting factors

-coumarin, warfarin (coumadin)

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aspirin

-suppresses thromboxane A₂

-other anticoagulants discovered in animal research

-medicinal leeches used since 1884 (hirudin)

-snake venom from vipers (arvin)

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streptokinase

-enzyme made by streptococci bacteria

-used to dissolve clots in coronary vessels

-digests almost any protein

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tissue plasminogen activator (TPA)

works faster, is more specific, and now made by transgenic bacteria

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hementin

produced by giant Amazon leech

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pericardium

-double-walled sac that encloses the heart

-allows heart to beat w/o friction, provides room to expand, yet resists excessive expansion

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parietal pericardium

-superficial fibrous layer of connective tissue

-deep, thin serous layer

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visceral pericardium (epicardium)

-serous membrane covering heart

-adipose in thick layer in some places

-coronary blood vessels travel through this layer

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pericarditis

painful inflammation of the membranes

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endocardium

-smooth inner lining of heart and blood vessels

-covers the valve surfaces and is continuous with endothelium of blood vessels

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fibrous skeleton of the heart

-framework of collagenous and elastic fibers

-provides structural support and attachment for cardiac muscle and anchor for valve tissue

-electrical insulation between atria and ventricles; important in timing and coordination of contractile activity

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atrioventricular sulcus

separates atria and ventricles

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interventricular sulcus

-overlies the interventricular septum that divides the right ventricle from the left

-contain coronary arteries

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pectinate muscles

internal ridges of myocardium in right atrium and both auricles

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trabeculae carneae

-internal ridges in both ventricles

-may prevent ventricle walls from sticking together after contraction

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ventricles relax

-pressure drops inside the ventricles

-semilunar valves close as blood attempts to back up into the ventricles from the vessels

-AV valves open

-blood flows from atria to ventricles

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ventricles contract

-AV valves close as blood attempts to back up into the atria

-pressure rises inside of the ventricles

-semilunar valves open and blood flows into great vessels

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angina pectoris

-chest pain from partial obstruction of coronary blood flow

-pain caused by ischemia of cardiac muscle

-obstruction partially blocks blood flow

-myocardium shifts to anaerobic fermentation, producing lactate and thus stimulating pain

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myocardial infarction (MI)

-sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation

-responsible for about 27% of all deaths in the U.S.

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mechanical junctions

tightly join cardiomyocytes

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