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Human Physiology 2 > Ch. Nine: Blood > Flashcards

Ch. Nine: Blood Flashcards

1
Q

Functions of the Blood

A
  • transport, defense, and hemostasis
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2
Q

Blood Characteristics

A
  • 8% of body weight
  • makes up 25% of extracellular fluid
  • blood is thicker than water: contains 3 cell types and suspended in plasma
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3
Q

Types of Cell Types

A
  • erthrocytes: RBCs
  • leukocytes: WBCs (immune system’s mobile defence units)
  • platelets: thrombocytes (cell fragments and important in hemostasis)
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4
Q

Haematocrit

A
  • centrifuge blood to separate cells from plasma
  • 99% are RBCs
  • hematocrit (packed cell volume) is 42% for women and 45% for men
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5
Q

Plasma

A
  • fluid portion of blood
  • 92% water and 7% proteins
  • remaining 1%: dissolved organic molecules, ions, and trace elements, vitamins, dissolved o2 and co2
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6
Q

Plasma Proteins

A
  • remain in the blood; most made in liver and colloid osmotic pressure (remember bulk flow)
  • 3 major groups: Albumins, Globulins, and Fibrinogen
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7
Q

Albumin

A
  • most prevalent: 60% of total, contribute to colloid osmotic pressure
  • bind many substances: bilirubin and drugs
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8
Q

Globulins

A
  • alpha, beta, and gamma
  • alpha and beta: transport hormones and cholesterol, and involved in blood clotting
  • are inactive before regulatory inputs: Angiotensinogen
  • y= immunoglobulins (antibodies)
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9
Q

Fibrinogen

A
  • forms fibrin threads essential to blood clotting
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10
Q

Erythrocytes

A
  • transport O2 to tissues and remove CO2
  • thin, biconcave disks which provides large surface area for diffusion of oxygen
  • very flexible can squeeze into capillaries
  • no nucleus nor organelles
  • glycolytic enzymes
  • carbonic anhydrase
  • hemoglobin (binds oxygen and carbon dioxide)
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11
Q

Hemoglobin (Hb)

A
  • found only in red blood cells
  • pigment containing iron: appears reddish when oxyengenated
  • molecule consists of 2 parts:
    1. Globin portion: protein composed of four highly folded polypeptide chains
    2. Heme groups: 4 iron groups per Hb molecule, each is bound to one of the polypeptides
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12
Q

Primary Role of Hemoglobin

A
  • carry O2

- also combines with CO2, H+ from CO2 reaction (not on heme group), carbon monoxide, and nitric oxide

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13
Q

Erythrocytes Enzymes

A
  • glycolytic enzymes: anaerobic respiration, and rely on glycolysis for ATP formation
  • carbonic anyhdrase: critical in CO2 transport, catalyzes reaction that leads to conversion of metabolically produced CO2 into bicarbonate ion (primary form in which CO2 is transported in blood)
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14
Q

Erythropoiesis

A
  • erythrocyte production
  • RBCs survive about 120 days
  • spleen removes most of old erythrocytes from circulation (1% per day)
  • must be replaced at rate of 2 million to 3 million cells/second
  • erythropoiesis occurs in red bone marrow: stem cells in red bone marrow differentiate into the different types of blood cells
  • production controlled by erthropoitin from kidney on demand
  • cells committed to becomes RBCS proliferation and maturation
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15
Q

Erythropoiesis in Age

A
  • intrauterine: first by yolk sac, developing liver and spleen, and bone marrow when developed
  • childhood: most bones have red bone marrow
  • adulthood: sternum, ribs, upper ends of long bones
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16
Q

Blood Types

A
  • special case of active immunity
  • ABO blood types are named for presence of antigens on surface of erythrocytes
  • type A: contains A antigens
  • type B: contains B antigens
  • type AB: contains both A and B antigens
  • type O: neither A or B antigens
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17
Q

Blood Groups

A
  • antibody binds with the specific antigen against which its produced
  • type A has anti-B antibodies (plasma)
  • type B has anti-A antibodies (plasma)
  • type AB has no antibodies related to the ABO system
  • type O has both anti-A and anti-B antibodies (plasma)
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18
Q

Blood Groups: transfusion

A
  • transfusion reaction occurs when blood of incompatible type is given
  • type O is “universal donar”
  • type AB is “universal recipient’
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19
Q

Transfusion Reaction

A
  • most dangerous is AB in recipient’s plasma for incoming donor RBCs
  • high HB my cause kidney failue
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20
Q

Rh Blood Group

A
  • people who have Rh factor have Rh-positive blood
  • no naturally occurring antibodies develop against Rh factor
  • anti-Rh antibodies are produced only by Rh-negative people if exposed to Rh-positive blood
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21
Q

Rh Factor

A
  • erythroblastosis fetalis (hemolytic disease of newborn) in subsequent pregnancies
  • rH-negative mother develops antibodies against the erythrocytes of an Rh-positive fetus
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22
Q

Other Blood Group Systems

A
  • cross-matched blood: mix donor RBCs with plasma of recipient
  • approx. 12 other minor human erythrocyte antigen systems
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23
Q

Filtering and Destruction of Erythrocytes

A
  • spleen filters and removes old erythrocytes
  • liver metabolizes byproducts from breakdown of erythrocytes
  • iron is recycled for synthesis for new hemoglobin and transported bound to transferrin to red bone marrow
  • iron is stored to ferritin in the liver, spleen, and small intestines
24
Q

Spleen

A
  • spleen macrophages filter blood by phagocytosis of old fragile RBCs
  • hemoglobin broken down and the iron is removed
  • converted into bilirubin (yellow colour)
  • further metabolism in liver: secreted in bile to the intestinal tract or released into the blood stream and excreted in the urine
25
Q

Anaemia

A
  • below-normal O2-carrying capacity
  • nutritional anaemia: iron deficiency in diet
  • pernicious anaemia: vitamin B12 deficiency (required for action of folic acid), dietary (only form animal products), and lack of intrinsic factor from stomach lining
  • aplastic anaemia: insufficient RBC production, or destruction of bone marrow (radiation, cancer, or chemotherapy)
  • renal anaemia: kidney disease or failure
  • hemorrhagic: wound or menstral flow
    Hemolytic anaemia: rupture of RBCs caused by infections (malaria) or sickle cell disease (fragile and production unable to keep up with removal)
26
Q

Polychthaemia

A
  • primary polycthaemia: erythropoiesis at excessive and uncontrolled rate and viscosity of blood increased
  • secondary polychthaemia: adaptive mechanism- reduced O2 due to high altitude or chronic lung disease or heart failure
27
Q

Leukocytes

A
  • mobile units of body’s immune defense system
  • immune system: made up of leukocytes and variety of plasma proteins; recognizes and destroys material within body that are foreign to “normal self”
28
Q

Leukocytes Functions

A
  • defends against invading pathogens
  • identifies and destroys cancer cells that arise in body
  • functions as “cleanup crew” that removes worn-out cells and tissue debris
29
Q

Leukocytes Characteristics

A
  • colourless, lack hemoglobin
  • vary in structure, function and number
  • somewhat larger than RBCs
  • 5 different types: neutrophils, eosinophils, basophils, monocytes, and lymphocytes
  • characterized by appearance of nuclei and granules
  • names based on granuole-staining dyes
30
Q

Leukocytes Production

A
  • ultimately originate form same undifferentiated multipotent stem cells in red bone marrow
  • granulocytes and monocytes are produced only in bone marrow
  • most new lymphocytes are actually produced by lymphocytes already in lymphoid tissues such as lymph nodes and tonsils
31
Q

Granulocytes

A
  • ctyoplasmic granules: neutrophils, eosinophils, and basophils
  • many shaped nucleus
32
Q

Agranulocytes

A
  • no ctyoplasmic granules: monocytes, and lymphocytes

- single nucleus

33
Q

Polymorphonucleur granulocytes

A
  • neutrophils: granules are neutral and show no dye preference
  • eosinophils: granules have an affinity for the red dye eosin
  • basophils: granules have an affinity for a basic blue dye
34
Q

Mononuclear Agranulocytes

A
  • monocytes: have an oval or kidney-shaped nucleus

- lymphocytes: smallest of the leukocytes; usually have large spherical nucleus that occupies most of the cell

35
Q

Leukopoiesis

A
  • chemical messages from damaged or invaded tissues
  • colony-stimulating factors from endothelial cells, marrow fibroblasts, activated WBCs
    ex. granulocyte colony-stimulating factor: increased replication of granulocytes, especially neutrophils
36
Q

Neutrophils

A
  • phagocytic specialists: destroy bacteria by phagocytosis and also release bacteria-killing chemicals
  • functions: first defenders on scene of bacterial invasion, important in inflammatory response, scavenge to clean up debris, and increased cell count may point to bacterial infection
37
Q

Eosinophils

A
  • increase in circulating eosinophils is associated with:
  • allergic conditions such as asthma and hay fever
  • internal parasite infestations such as worms (attach to worms and secrete substances to kill it)
38
Q

Basophils

A
  • least numerous and most poorly understood
  • quite similar and functionally to mast cells
  • synthesize and store histamine (release in allergic reactions) and heparin (anti-clotting agent of blood samples drawn for chemical analysis, used extensively as anticoagulant drug)
39
Q

Monocytes

A
  • phagocytic:
  • migrate to tissues and become macrophages
  • also for antigen presentation, cytokine production and cytotoxicity
  • emerge from bone marrow while still immature and circulate for day or two before settling down in various tissues in body
  • mature and enlarge in resident tissue and become known as macrophages (life span from several months to years)
40
Q

Lymphocytes

A
  • B cells: produce antibodies and responsible to antibody-mediated or humoral immunity
  • T cells: bind to antigens and destroys cells (virus infected, cancer cells, tissue transplant) by releasing chemicals to punch holes in victim cell (cell-mediated immunity)
  • provide immune defense against targets for which they are specifically programmed
  • live about 100-300 days
41
Q

Platelets

A
  • from megakaryocytes
  • do not leave blood as WBCs do but (1/3) are stored in blood-filled spaces in spleen and released when needed by sympathetically induced splenic contraction
  • thrombopoietin: liver hormone increases number of megakaryocytes and more platelets per cell (mechanism unknown)
  • cytoplasmic fragments derived from megakaryocytes (1000 platelets/cell and last 10 days)
  • no nuclei, some organelles and enzymes
  • have granules important in blood clotting
  • granules contain secretory products: ADP, sertonin, and epinephrine
42
Q

Haemostasis

A
  • stoppage of bleeding from broken blood vessel
  • haemostasis is a 3 step process:
    1. vascular spams
    2. formation of platelet plug
    3. blood coagulation
43
Q

Vascular Spasm

A
  • results from damage to the blood vessel; damaged tissue secretes factors that cause contraction
  • vessels constrict to minimize blood loss (maintains BP)
  • endothelial layer becomes sticky to aid in the clotting process
44
Q

Formation of Platelet Plug

A
  • platelet aggregate on contact with exposed collagen in damaged wall of the vessel
  • forms a sticky endothelium and exposed collagen- platelet activation
  • release ADP which causes platelets to become sticky- platelet aggregation
  • thromboxane A2 synthesis from activated platelets stimulate further platelet aggregation
  • the plug results in a decreased blood loss (maintains BP)
  • plug formation is important for production of a blood clot
45
Q

Formation of Blood Clot

A
  • clotting= coagulation
  • blood converted into solid gel called clot or thrombus
  • occurs around platelet plug
  • dominant hemostatic defence mechanism: can take place in absence of all cells except platelets
46
Q

Clot Formation

A
  • reinforces platelet plug and converts blood in the vicinity of vessel injury into a nonflowing gel
  • clotting factors are always present in blood plasma in inactive precursor form; activated in a cascade
47
Q

Clotting Cascade

A
  • 12 plasma proteins produced mainly in the liver:
  • designated with roman numerals (and names) and act as proteolytic enzymes or co-factors
  • series of steps lead to final conversion of fibrinogen into a stabilized fibrin mesh
  • may be triggered by intrinsic or extrinsic pathway
  • fibriogen converted to fibrin by thrombin
48
Q

Clotting Cascade: Summary

A
  • intrinsic pathway: all elements present in blood:
  • involves seven separate steps
  • factor XII (Hageman factor) is activated by coming into contact with exposed collagen in injured vessel
  • or foreign surface such as glass test tube
  • extrinsic pathway:
  • requires only 4 steps
  • requires contact with tissue factors external to the blood
  • tissue thromboplastin released from traumatize tissue directly activates factor X
49
Q

Clot Retraction and Dissolution

A
  • clot retraction: contraction of platelets shrinks fibrin mesh, squeezing fluid from the clot
  • clot dissolution: enzyme plasmin dissolves clot and plasmin formed from plasminogen
50
Q

Dissolving Blood Clots- Factor XII

A
  • plasminogen converted to plasmin; fibrinolytic enzyme

- breaks down the fibrin meshwork

51
Q

Plasminogen Activators

A
  • plasminogen activators convert plasminogen to plasmin:
    ex. tissue plaminogen activator (tPA); secreted by endothelial cells especially in lungs, plasminogen and tPA bind to fibrin
  • recombinant tissue plasminogen activator (tPA):
  • dissolve clots that are obstructing flow in coronary arteries, pulmonary arteries and cerebral arteries
  • used to treat stroke patients if they arrive soon enough to the hospital
52
Q

Clot Controllers

A
  • swift removal of clotting factors and inhibition of active clotting factors:
  • most of the thrombin is bound to the fibrin threads thus prevents systemic clotting
  • unbound thrombin is inactivated
  • endothelial cells:
  • nitric oxide, prostacyclin, endothelial dysfunction
53
Q

Inappropriate Clotting

A
  • thrombus:
  • abnormal intravascular clot attached to a vessel wall
  • can eventually completely occlude the vessel
  • ischemia and tissue death downstream from the clot ex. fatal heart attacks
  • emboli:
  • freely floating clots
  • can suddenly block blood flow
  • pulmonary embolism impair the body’s ability to get enough oxygen
  • cerebral embolisms cause strokes
54
Q

Thromboembolic Conditions

A
  • factors that can cause thromboembolism:
  • roughened vessel surface associated with atherosclerosis
  • imbalances in the clotting-anticlotting systems
  • slow-moving blood
55
Q

Role of Coagulation Factors in Clot Formation Disorders

A
  • impaired liver function: reduced protein production including clotting factors
  • vitamin K deficiencies: decreased synthesis of clotting factors
56
Q

Hemophillia: FYI

A
  • genetic X-linked disorders seen primarily in men
  • Hemophilia A is a lack of factor VIII
  • hemophillia B is lack of factor IX
  • hemophillia C can be seen in both sexes and is milk; kacks factor XI
  • symptoms occur early in life and can be disabling

Human Physiology 2 (10 decks)

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