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Anat/Phys > Chapter 16: Blood > Flashcards

Chapter 16: Blood Flashcards

0
Q

Blood

A

Specialized kind of connective tissue in which formed elements- living cells - are suspended in a non-living fluid matrix (plasma).

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1
Q

Blood route

A

Heart-arteries-capillaries-body tissues (blood releases O2 & nutrients; picks up CO2 and wastes)-Veins-Heart-lungs-heart- body

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2
Q

Centrifuged blood splits into top to bottom

A
  1. Plasma
  2. Buffy-coat WBC & platelets
  3. Red blood cells
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3
Q

Functions of blood

A
  1. Distribution
  2. Regulation
  3. Protection
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5
Q

Distribution of blood

A
  1. Deliver oxygen & nutrients to all body cells
    2 . Takes waste (CO2 & metabolic wastes) from cells to areas if elimination (eg. Lungs, kidneys)
  2. Transports hormones from endocrine organs to target areas.
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6
Q

regulation

A
  1. maintains body temp; absorbs and distributes heat throughout the body and to skin surface to encourage heat loss.
  2. helps maintain normal pH; proteins and other solutes in the blood act as buffers to serious changes in pH that could be detrimental and blood holds a reserve of bicarbonate atoms
  3. helps maintain adequate fluid volume for circulatory system; Salts and blood proteins act to prevent excessive blood loss from bloodstream into tissues
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7
Q

protection

A
  1. preventing blood loss; platelets and plasma initiate clotting
  2. preventing infection; antibodies, complement proteins and WBC defend the body against bacteria and viruses.
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8
Q

% water in blood

A

90%

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9
Q

blood plasma composition is maintained by …

A

liver, respiratory system and kidneys

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10
Q

3 types of blood cells/ formed elements

A
  1. white blood cells - leukocyte -only true cell
  2. red blood cell- erythrocyte
  3. thrombocyte-platelets
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11
Q

3 structural characteristics for RBC’s function of gas transport

A
  1. small size and biconcave shape- allows for large surface area to volume
  2. over 97% hemoglobin (discounting water content)- hemoglobin binds to a transports respiratory gases
  3. lack of mitochondria and generation of ATP by anaerobic mechanisms-
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12
Q

more RBCs in blood , visocity is

A

higher, slower the blood

- fewer RBC -lower viscosity- faster the blood

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13
Q

function of RBC

A

-transporting respiratory gases

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14
Q

Hemoglobin

A

-protein makes RBC’s red, this binds easily & reversibly with oxygen

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15
Q

hemoglobin structure

A
  • major: globin protein with 2 alpha and beta chains - 4 chains, each attached to a heme pigment - each has IRON FE2 core
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16
Q

each iron molecule can attach to one O2 molecule, so how many O2 can each hemoglobin molecule transport?

A

4 oxygen molecules

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17
Q

hemoglobin function in lungs

A
  • in lungs: O2 diffuses from the air sacs of the lung into the lungs into the blood and goes to bind to the iron in hemoglobin, it changes its shape and forms oxyhemoglobin, blood is then bright red.
  • less oxygen- blood is dark red
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18
Q

hemoglobin function in tissues

A
  • in tissues: hemoglobin releases O2 and resumes its normal shape becoming deoxyhemoglobin
  • CO2 then binds to the amino acids of hemoglobin, forming carbaminohemoglobin to be carried back to the lungs for elimination.
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19
Q

production of erythrocyte

A
  1. HEMATOPOIESIS- blood cell formation; occurs in red bone marrow . about an ounce of blood with 100 billion new cells are produced every day
  2. HEMOCYTOBLAST AKA hematpoietic stem cell-cell that are precursors to your blood cells of all types-reside on red bone marrow
  3. ERYTHROPOIESIS- hemocytoblast- myeloid stem cell- proerythroblast - early (basophilic) erythroblasts ( synthesize ribosomes) -late erythroblasts (starting to accumulate hemoglobin)- reticulocyte (start to lose nucleus)- erythrocyte
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20
Q

reticulocyte

A

-rough idea of rate of RBC formation

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21
Q

requirements for regulation of RBC

A
  • too few RBC- not enough O2

- too many- blood that is too thick

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22
Q

erythropoietin EPO

A
  • direct hormonal stimulus for creating RBC production
  • EPO is produced by the kidneys & liver; so when kidney cells become low on O2 (hypoxic), the signaling molecule HYPOXIA-INDUCIBLE FACTOR. HIF is no longer broken down.
  • accumulation of HIF speeds up the production/release of erythropoietin
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23
Q

drop in O2 that triggers EPO release results from:

A
  1. lower number of RBC due to hemorrage (bleeding out) or excessive RBC destruction
  2. Don’t have enough hemoglobin per RBC
    - iron deficiency
  3. low oxygen-at high altitude of during pneumonia
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24
Q

epo stimulates red marrow cells commited to becoming erythrocytes to….

A

mature more rapidly

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25
Q

synthetic EPO

A

-increases RBC production, could be used as athlete enhancement steroid

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26
Q

testosterone

A
    • other chemicals can stimulate RBC production
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27
Q

Dietary reqs for RBC

A
  • IRON is essential for erythropoiesis to form hemoglobin(contains 65% of body’s iron stores)
  • free iron is toxic , so extra iron is stored as a protein iron complex in the stored in liver, spleen or bone marrow
  • vitamins needed for DNA synthesis incl. Vit B12 and Folic Acid
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28
Q

RBC life span

A

100-120 days

why? They don’t have nucleus or organelles , thus can’t make new proteins for repair, when things break down cell dies.

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29
Q

why is spleen AKA RBC graveyard?

A
  • fragmented dying RBC tend to get trapped in small circulatory channels commonly found in spleen
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30
Q

When macropages engulf dying RBC, how is it broken down?

A
  • HEME is split from GLOBIN and IRON is stored for reuse
  • the rest of the HEME is degraded to BILIRUBIN, which is picked up by the liver, transported in bile to the intestine and ultimately released as a brown pigment in feces
  • the GLOBIN part is metabolized or reused
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31
Q

erythrocyte disorders-Anemias

A

blood has abnormally low capacity to carry O2 , you get pale , short of breath (lungs try to compensate for lack of O2)

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32
Q

Common causes for anemia

A
  1. insufficient # of RBCs
  2. Low hemoglobin
  3. Abnormal hemoglobin
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33
Q

hemorrhagic anemia

A
  • blood loss-rapid(ex. stab wound)

- or gradual overtime (bleeding ulcer)-loss of more blood overtime

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34
Q

hemolytic anemia

A
  • RBC lyse prematurely, takes on too much water, or mismatched blood transfusion, hemoglobin abnormality, or certain bacterial or parasitic infections that cause cells to break down
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35
Q

aplastic anemia

A
  • destruction of red bone marrow

- by chemicals, rediation, viruses, side effect of chemo(bone marrow cancer)

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36
Q

iron deficiency anemia

A
  • not enough iron in diet, loose all your blood

- RBCs produced called MICROCYTES are small and pale

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37
Q

pernicious anemia

A
  • vitamin B12 deficiency , could be mutation of factor to breakdown B12 , can’t process
  • developing RBCs grow but don’t divide, resulting in large pale cells called MACROCYTES
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38
Q

thalassemias

A
  • you have a missing or faulty globin chain

- you would need blood transfusions

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39
Q

sickle-cell anemia

A
  • alteration of a single amino acid in a beta chain of the globin molecule causes beta chains to link under low O2 condtiions and the RBCs become crescent shaped
  • Results: rupture easily & don’t deliver oxygen very well
  • 2 allele disease - partial sickle - can’t get malaria -become carrier
  • fetal hemoglobin won’t sickle and other treatments are stem cell transplants and gene therapy
40
Q

Polycythemia

A
  • abnormal excess of RBC , blood is very thick
41
Q

polycythemia vera

A
  • bone marrow cancer, very high RBC count, don’t die but undergo crazy division
42
Q

secondary polycythemias

A

people in higher altitudes, your body compensates naturally, not high enough to be dangerous

43
Q

blood doping

A

-athlete will take out RBCs from body a few days before event and re-inject on event day

44
Q

Leukocyte general structure and function

A
  • complete cells with nucleia and organelles
  • avg. 4800-10,800 WBC/micrliter of blood-(many fewer than RBC 4-5 mill)
  • defense against bacteria, viruses, parasites, toxins and tumor cells
45
Q

diapedesis

A

where WBC leave the blood stream through blood vessels, they go to places of injury

46
Q

amoeboid motion

A

-WBC use cytoplasmic extensions to move themselves

47
Q

positive chemotaxis

A

WBC follow a chemical trail left by bacteria or damaged cells or other WBCs to act to injured or damaged area

48
Q

leukocytosis

A

WBC count that is over 11,000 cells per microliter, indicates you have infection

49
Q

granulocytes vs. agranulocytes

A

-if they have membrane bound organelles or not

50
Q

order of abundance most to least

A
  • Never-neutrophils
  • Let - lymphocytes
  • Monkeys- monocytes
  • Eat- eosinophils
  • Bananas- basophils
51
Q

Leukemia

A
  • WBCs remain unspecialized and proliferate out of control; take over red bone marrow and crowding out other blood cells
  • symptoms: severe anemia & bleeding, fever, weight loss and bone pain
  • treatments: Irradiation, chemotherapy to destroy the dividing cells
52
Q

Infectious Mononucleosis

A
  • caused by the Epstein-Barr virus and marked by excessive numbers of agranulocytes
  • symptoms: tiredness, aches, chronic sore throat & low grade fever
  • condition resolves itself in a few days- transmissible thru saliva
53
Q

leukopenia

A

abnormally low WBC count commonly induced by drugs such as glucocorticoids and anticancer agents

54
Q

leukopoiesis

A

-stimulated by chemical messengers called interleukins and colony stimulating factors

55
Q

granulocyte life span

A
  • only about less than 1 day to 9 days

- they die combating microorganisms-kill themselves in order to kill bacteria- suicide bombers

56
Q

platelets

A
  • cytoplasmic fragments of very large cells called MEGAKARYOTES; 150,000-400,000 /ul of blood
  • essential for clotting that occurs when blood vessels are ruptured or otehrwise injured
  • don’t have nucleus and live a short time, around 10 days
57
Q

thrombopoietin

A

-hormone regulates production of platelets

58
Q

hemostasis

A

stoppage of bleeding

59
Q

3 steps of hemostatis

A

1) vascular spasm
2) platelet plug formation
3) coagulation

60
Q

vascular spasm

A

smooth muscles in vessel constrict & that helps prevent blood loss, could be caused by injury of smooth muscle

61
Q

platelet plug formation

A
  • platelets start to aggregate and form a temporary plug
  • normally platelets are preventing from sticking to one another or to linings of blood vessels by chemicals
  • however, when endothelium is damaged, underlying collagen fibers are exposed and platelets adhere to these
  • when platelets aggregate they release chemical messengers like ADP, serotonin, thromboxane A2 which enhance platelet effects, leading to a positive feedback cycle
62
Q

coagulation

A
  • blood clotting reinforces the blood clot using Fibrin threads -platelet plug
  • in clotting blood is transformed from a liquid to a gel via multiple steps involving clotting factors, type of plasma proteins-Phase 1-3
63
Q

anticoagulents

A

inhibit clotting, normally found in blood, you want blood flowing freely

64
Q

clot retraction and repair

A

contractile proteins will pull the fibrin strands, squeezing SERUM(plasma- clotting protein) from mass , compacting the clot & drawing ruptured edges

65
Q

platelet derived growth factor (PDGF) and vascular endothelial growth factor(VEGF)

A
  • these stimulate cell division patch up area and repair any destroyed tissue
66
Q

fibrinolysis

A
  • removes uneeded clots when healing has occured
  • presence of a clot causes endothelial cells to secrete TISSUE PLASMINOGEN ACTIVATOR tPA which activates the plasma protein PLASMINOGEN which in turn produces the fibrin digestive enzyme PLASMIN
67
Q

factors limiting clot growth or formation

A
  1. 2 homestatic mechanisms prevent clots from becoming too large:
    a. swift removal of clotting factors-occurs in rapidly moving blood
    b. inhibition of activating clotting factors
  2. the smoothness of the endothelium and antithrombic chemicals usually prevent platelets from adhering when clotting is undesirable
68
Q

thromboembolic

A

undesirable clot formation

69
Q

thrombus

A

clot that develops & persists in an unbroken blood vessel

ex. coronary thrombus-causes heart attack -blocks blood supply to the heart

70
Q

embolus

A

thrombus freely floating in blood stream, can get stuck

ex. pulmonary embolism, can’t breath that well or cerebroembolism - block to the brain

71
Q

drugs that help prevent undesirable clotting

A
  • aspirin
  • heparin
  • warfarin
  • all act in different pathway of clotting
72
Q

Disseminated Intravascular Coagulation

A
  • widespread clotting occurs in intact blood vessels and residual blood becomes unable to clot
  • widespread bleeding occurs
  • most often encountered as a complication of pregnancy, septicemia, or incomplete blood transfusion
73
Q

bleeding disorders

A

-anything that interferes with normal clotting

74
Q

thrombocytopenia

A
  • not having enough platelets
  • even normal movement leads to widespread hemorrhage
  • arise from : cancer, radiation or drugs that destroy your red bone marrow
  • platelet count of less than SR is diagnostic
75
Q

impaired liver function

A

lead to bleeding disorder

  • liver is unable to produce procoagulants
  • severe bleeding occurs
  • can occur due to Vit K deficiency , can occur in new borns
76
Q

hemophilia

A

hereditary bleeding disorder, minor trauma can cause long term bleeding

77
Q

Hemophilia A

A
  • 77% of deficiencies, Factor 8 deficiency-antihemophilic

- X-linked

78
Q

Hemophilia B

A
  • deficiency of Factor 9

- X-linked

79
Q

Hemophilia C

A
  • less severe, lack of factor XI , seen in both sexes

treatment: blood transfusions or factor injections

80
Q

cardiovascular system minimizes effects of blood loss by:

A
  1. reducing the volume of affected blood vessels

2. stepping up the production of red blood cells

81
Q

loss of what __% cause pallor and weakness

A

15-30%

-loss of more than 30% volume results in severe shock, can be fatal

82
Q

whole blood transfusion

A
  • for rapid blood loss
  • infusion of PACKED RED CELLS , whole blood from which most of the plasma has been removed, if medium loss, will help you carry oxygen
83
Q

Antigens (agglutinigens)

A
  • blood type differentiation -ABO blood types based off this
  • glycoproteins on cell surface ; cell-cell recognition, cause destruction of cells that don’t have appropriate antigen present
84
Q

Antibodies(agglutinins)

A
  • exist in the plasma
  • attack antigens not present in persons own blood cells
    ex. blood type A will produce Antigens Anti-B antibodies
85
Q

transfusion reactions

A

-mismatched blood is infusion and the donors red blood cells will be attacked by the recipients plasma agglutinins

86
Q

what happens when foreign blood cells are attacked

A
  • when foreign blood cells are attacked and agglutinated (clumped) they are going to clog small vessels and later they are destroyed by phagocytes and their hemoglobin is released; the released hemoglobin can travel to the kidneys & cause renal failure
  • nonlethal symptoms incl: fever, chills , low blood pressure, rapid heart beat, nausea and vomiting
87
Q

blood typing

A
  • crossmatching tests are done to test for agglutination of donor RBCs by recipient’s serum
88
Q

restoring blood volume when death is imminent and there is no time to cross-match

A

-use saline or multiple-electrolyte solution, then replace RBCs later

89
Q

differential white blood cell count

A
  • look at % of each type of white blood cell

- ex. a high eosinophil count may indicate a parasitic infection or an allergic response somewhere in the body

90
Q

SMAC

A

-blood chemistry blood profile

91
Q

Complete Blood Count CBC

A
  • counts # of different formed elements, your hematocrit, your hemoglobin content and size of RBC
  • ex. platelet count can test for THROMBOCYTOPENIA, while hematocrit levels and difference in size/shape of RBCs could indicate iron deficiency or anemia
92
Q

location of fetal development of blood cells

A
  • blood cells form in sites such as liver & spleen

- by 7th month the red marrow is the primary hematopoietic area

93
Q

Hemoglobin F

A

-in fetus , this has higher affinity for oxygen (can bind more O2), sickle-cell anemia treatment

94
Q

most common blood diseases during aging

A
  • chronic leukemia
  • anemia
  • clotting disorders
    • this may be due to deficiencies in the heart, vessels and immune system
95
Q

hemocytoblast

A

AKA hemotopoetic stem cell-cells that are precursors to your blood cells of all types, reside in red bone marrow , can be WBC, RBC and platelete

96
Q

atherosclerosis

A

-or inflammation in the vessel endothelium can cause platelet buildup (clotting) as well as slowly flowing blood such as in a bedridden patient

Anat/Phys (15 decks)

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