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A+P 2 > chp 17. > Flashcards

chp 17. Flashcards

1
Q

Functions of Blood

A
  • transportation-
  • -oxygen from the lungs and nutrients from the intestine to all cells of the body
  • -Transport metabolic waste
  • -Transport hormones
  • regulation
  • -Distribute heat around body
  • -maintain pH, serve as a bicarbonate reserve
  • -maintain fluid volume
  • protection
  • -excess blood loss (creates blood clots)
  • prevent infection(white blood cells)
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2
Q

Spun tube of blood yields three layers:

A

Erythrocytes on bottom 45% of whole blood

WBCs and platelets in Buffy coat- less than 1%

Plasma on top-55%

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3
Q

Hematocrit

A

percent of blood volume that is RBCs

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4
Q

formed elements

A

Buffy coat, erythrocytes

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5
Q

bright red

dark red

A

oxygenated

deoxygenated

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6
Q

which gender has more blood

A

adult male 5-6L

adult female 4-5L

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7
Q

pH of blood

and temp

A

pH= 7.35-7.45= slightly alkaline

temp=100.4

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8
Q

Blood Plasma color and texture

  • mostly made up of
  • which are most abundant
A 
Straw colored, sticky
Water (90% of volume) 
100+ Dissolved solutes (hormones, ions, gases, etc.)
Proteins are the most abundant solutes
Albumin (60% of plasma protein)
Blood buffer
Shuttles molecules
Maintains osmotic pressure
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9
Q

Formed elements detailed

A 
-Erythrocytes (Red-blood cells)
Anucleate (without nucleus)
-Leukocytes (White-blood cells)
Nucleated 
-Platelets
Cell fragments
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10
Q

Erythrocytes description

-spectrin?

A
  • Bioconcave disk
  • –large surface area

-no nuclues

  • no organalles
  • -no O2 consumption
  • lots of hemoglobin
  • -caries o2, 97% HB

Spectrin
-a cool protein in the plasma membrane that lets the cell change shape

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11
Q

three characteristics of red blood cells that demonstrate form and function relationship

A

Three features make for efficient gas transport:

  • Biconcave shape offers huge surface area relative to volume for gas exchange
  • Hemoglobin makes up 97% of cell volume (not counting water)
  • RBCs have no mitochondria
  • -ATP production is anaerobic, so they do not consume O2 they transport
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12
Q

Hemoglobin consists of

A

red heme pigment bound to the protein globin

-Globin is composed of four polypeptide chains
Two alpha and two beta chains
-A heme pigment is bonded to each globin chain
Gives blood red color
Each heme’s central iron atom binds one O2

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13
Q

Each Hb molecule can transport

A

four oxygens

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14
Q

O2 loading in lungs

Produces

A

oxyhemoglobin (ruby red)

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15
Q

O2 unloading in tissues

Produces

A

deoxyhemoglobin, or reduced hemoglobin (dark red)

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16
Q

CO2 loading in tissues

A

20% of CO2 in blood binds to Hb, producing carbaminohemoglobin

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17
Q

word for production of RBC’s and where does it occur

A

Hematopoiesis (hemopoiesis) occurs in the Red Bone Marrow

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18
Q

All formed elements derived from the ____ cell

A

hematopoietic stem cell (hemocytoblast)

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19
Q

phases of RBC

A

hematopoietic stem cell->pro erythroblast->Basophilic erythroblast (phase 1)->polychromatic erythroblast->orthochromatic erythoroblats(phase 2)-> reticulocyte(phase 3)->erythrocyte

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20
Q

too few RBCs lead to

too many RBC lead to

A

Too few RBCs lead to tissue hypoxia

Too many RBCs increase blood viscosity

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21
Q

Balance between RBC production and destruction depends on:

A

Hormonal controls

Dietary requirements

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22
Q

Erythropoietin(EPO)

-relased by ____ in response to

A

hormone that stimulates formation of RBCs
-Always small amount of EPO in blood to maintain basal rate
-Released by kidneys (some from liver) in response to hypoxia
At low O2 levels, oxygen-sensitive enzymes in kidney cells cannot degrade hypoxia-inducible factor (HIF)
HIF can accumulate, which triggers synthesis of EPO

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23
Q

Causes of hypoxia:

A
  • Decreased RBC numbers due to hemorrhage or increased destruction
  • Insufficient hemoglobin per RBC (example: iron deficiency)
  • Reduced availability of O2 (example: high altitudes or lung problems such as pneumonia)
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24
Q

Too many erythrocytes or high oxygen levels in blood

A

inhibit EPO production

  • EPO causes erythrocytes to mature faster
  • -Testosterone enhances EPO production, resulting in higher RBC counts in males
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25
Q

Erythropoietin mechanism

A
  1. hypoxia-> kidney releases erythropoietin-> erythropoietin stimulates red bone marrow->enhanced erythropoiesis increases RBC count-> O2-carrying ability of blood rises
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26
Q

Some athletes abuse artificial EPO
Use of EPO
Dangerous consequences:

A

-increases hematocrit, which allows athlete to increase stamina and performance

  • EPO can increase hematocrit from 45% up to even 65%, with dehydration concentrating blood even more
  • Blood becomes like sludge and can cause clotting, stroke, or heart failure
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27
Q

Dietary requirements for erythropoiesis

A
  • Amino acids, lipids, and carbohydrates
  • Iron: available from diet
  • -65% of iron is found in hemoglobin, with the rest in liver, spleen, and bone marrow
  • -Free iron ions are toxic so iron is bound with proteins:
  • —Stored in cells as ferritin and hemosiderin
  • —Transported in blood bound to protein transferrin
  • Vitamin B12 and folic acid are necessary for DNA synthesis for rapidly dividing cells such as developing RBCs
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28
Q

RBC’s lifespan

RBC’s engulfed by macrophages

A

Useful life span of 100-120 days

  • often trapped in spleen
  • Iron core recycled
  • Heme group degraded to bilirubin and taken to liver
  • -Secreted in bile and lost
  • Globin protein metabolized for its amino acids
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29
Q 
Anemia
Hemmorgic
HEMOLYTIC
Aplastic
Iron deficiency
Pernicious
Thalassemias
Sickle cell
Polycythemia
A

low oxygen carrying capacity of blood

  • Insufficient number of cells
  • –Hemmoragic: rapid blood loss
  • –Hemolytic: rupture of RBC’s (infection, etc)
  • -Aplastic: bone marrow impaired
  • Decreased hemoglobin content
  • -Iron deficiency (creating microcytes-small pale RBCs)
  • -Pernicious: deficiency of B12 (intrinsic factor needed for absorption of vitamin, macrocysts-large pale RBCs)
  • Abnormal hemoglobin
  • -Thalassemias: faulty globin chains
  • -Sickle cell anemia: Change in the beta chain of HbS
  • -Polycythemia: excess of RBC’s,
  • —-Sometimes due to bone marrow cancer
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30
Q

leukocytes percentage of blood

A

less than 1% of blood

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31
Q

Leukocytes function

A

Defense against disease

32
Q

diapedesis

A

Leukocytes Able to pass through capillary beds (diapedesis), and move about tissues using amoeboid motion and positive chemotaxis

33
Q

Classes of Leukocytes

A 
Granulocytes- all phagocytic-
Cells have visual granules in 
	cytoplasm
-Neutrophils
-Basophils
-Eosinophils
Agranulocytes
-Lack visual granules in 
	cytoplasm
-Lymphocytes
-Monocytes
34
Q

Neutrophils

A
  • Very phagocytic
  • Most abundant
  • 2X size of RBC
  • Dye both red and blue
  • Granules hold defensins
  • -antibiotics
  • -Specialize in destroying bacteria
  • Nuclei 3-6 lobes (polymorphonuclear)
35
Q

Eosinophils

A

-2-4% of all WBC’s
-Bilobed nucleus
-Stain Red
-Granules hold digestive enzymes
—Defense against parasites
(tapeworms,roundworms, etc)
-too large to be phagocytized
-Role in allergies and asthma

36
Q

Basophils

A
  • 0.5% of all WBC’s; rarest type of WBC
  • Bilobed nucleus
  • Stains blue with addition of dye
  • Release histamine to attract further WBC’s to infected area
37
Q

Lymphocytes

A
  • Second most numerous WBC
  • Large, Spherical nucleus
  • Most in tissues, few in bloodstream
  • T-lymphocytes: act directly against virus infected cells and tumors
  • B-lymphocytes: give rise to plasma cells, which produce antibodies
38
Q

Monocytes

A
  • 3-8% of WBC’s
  • Largest WBC
  • U shaped nucleus
  • Macrophage function (swallow infected cells) and activate lymphocytes
  • Leave circulation and become macrophages
  • Very hungry
39
Q

Leukopoiesis

A
  • production of WBCs are stimulated by two types of chemical messengers from red bone marrow and mature WBCs
  • –Interleukins are numbered (e.g., IL-3, IL-5)
  • –Colony-stimulating factors (CSFs) are named for WBC type they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
40
Q

All leukocytes originate from

A

hemocytoblast stem cell that branches into two pathways:

  • Lymphoid stem cells produces lymphocytes
  • Myeloid stem cells produce all other elements
41
Q

Granulocyte production:
stored more in bone or blood?
which are formed more WBC or RBCs?

A
  1. Myeloblasts: arise from myeloid line stem cells
    - 2.Promyelocytes: accumulate lysosomes
  2. Myelocytes: accumulate granules
    - 4.Band cells: nuclei form curved arc
  3. Mature granulocyte: nuclei become segmented before being released in blood

10× more are stored in bone marrow than in blood
3× more WBCs are formed than RBCs, because WBCs have a shorter life, cut short by fighting microbes

42
Q

Agranulocyte production:

A

Monocytes: derived from myeloid line

  • Monoblast → promonocyte → monocyte
  • Share common precursor with neutrophils
  • Can live for several months

Lymphocytes: derived from lymphoid line

  • T lymphocyte precursors give rise to immature T lymphocytes that mature in thymus
  • B lymphocyte precursors give rise to immature B lymphocytes that mature within bone marrow
  • Lymphocytes live from a few hours to decades
43
Q

Platelets are formed from

Platelets function in?

A

Large cytoplasmic fragments broken off of megakaryocytes

  • Megakaryocytes are formed when mega karyoblasts undergo repeated mitosis without cytokinesis
  • regulated by thrombopoietin
  • Function in blood clotting
44
Q

Leukocyte disorders
Leukopenia
Leukemia
Infectious mononucleosis

A

-Leukopenia: low WBC’s (anti-cancer drugs)

  • Leukemia: impair normal bone marrow function
  • -Over production of abnormal WBC (usually cloning of a single abnormal cell)
  • -Acute: fast (from lymphoblasts)
  • -Chronic: slow (from myelocytes)

-Infectious mononucleosis: viral disease from the Epstein-barr virus. No cure. Rarely fatal

45
Q

Formation of Platelets

A

hematopoietic stem cell-> Megakaryoblast-> Megkrayocyte-> Megakaryocyte(bigger)-> platelets

46
Q

Control of bleeding

3 steps

A

Vascular spasm-smooth muscle contracts, causing vasoconstriction

Platelet plug formation-injury to lining f vessel exposes collagen fibers: platelets adhere, platelets release chemicals that make nearby platelets sticky; platelet plug forms

Coagulation-fibrin forms a mesh that traps red blood cells and platelets, from forming the clot

47
Q

Vascular spams are triggered by

A

Direct injury to vascular smooth muscle
Chemicals released by endothelial cells and platelets
Pain reflexes

  • most effective in smaller blood vessels
  • can significantly reduce blood flow until other mechanisms can kick in

-vasoconstriction

48
Q

prostacyclins and nitric oxide

A

secreted by endothelial cells act to prevent platelet sticking

-Platelets do not stick to intact vessel walls because collagen is not exposed

49
Q

_____factor helps to stabilize platelet-collagen adhesion

A

Von Willebrand

50
Q

When activated, platelets swell, become spiked and sticky, and release chemical messengers:
-uses what cycle

A
  • ADP causes more platelets to stick and release their contents
  • Serotonin and thromboxane A2 enhance vascular spasm and platelet aggregation

-Positive feedback cycle: as more platelets stick, they release more chemicals, which cause more platelets to stick and release more chemicals
Platelet plugs are fine for small vessel tears, but larger breaks in vessels need additional step

51
Q

Coagulation (blood clotting) reinforces platelet plug with fibrin threads in what kind of vessels?:
Blood is transformed from

A

Blood clots are effective in sealing larger vessel breaks

-liquuid to gel

52
Q

Coagulation forms in three phases: phase 1

A

Phase 1: Two pathways to prothrombin activator
Initiated by either intrinsic or extrinsic pathway (usually both)
-Triggered by tissue-damaging events
-Involves a series of procoagulants
-Each pathway cascades toward and ends with the activation of factorX

FactorX then complexes with Ca2+, PF3 (platelet factor 3), and factorV to form prothrombin activator

53
Q

Intrinsic pathway (coagulation)

A
  • Called “intrinsic” because clotting factors are present within the blood
  • Triggered by negatively charged surfaces such as activated platelets, collagen, or even glass of a test tube
54
Q

Extrinsic pathway

coagulation

A
  • Called “extrinsic” because factors needed for clotting are located outside blood
  • Triggered by exposure to tissue factor (TF); also called factorIII
  • Bypasses several steps of intrinsic pathway, so faster pathway
55
Q

Phase 2: Pathway to thrombin

coagulation

A

Prothrombin activator catalyzes transformation of prothrombin to active enzyme thrombin

56
Q

Phase 3: Common pathway to the fibrin mesh

A
  • Thrombin converts soluble fibrinogen to fibrin
  • Fibrin strands form structural basis of clot
  • Fibrin causes plasma to become a gel-like trap catching formed elements
  • Thrombin (along with Ca2+) activates factor XIII (fibrin stabilizing factor), which:
  • -Cross-links fibrin
  • -Strengthens and stabilizes clot
  • Anticoagulants: factors that normally dominate in blood to inhibit coagulation
57
Q

Thrombocytopenia

A

deficiency in the number of platelets

58
Q

Impaired liver function

A

unable to synthesize procoagulants. Often due to a Vitamin K problem

59
Q

Hemophilia:

A

hereditary bleeding disorder

  • Factors VIII (type A), IX (type B)
  • Sex linked (males get it more often)
  • Exercise can cause bleeding in joints
60
Q

Thrombus

A

Clot in an unbroken blood vessel

61
Q

Embolus

A

Thrombus floating through blood vessel

62
Q

Embolism

A

Embolus in a blood vessel too narrow for it to pass through

63
Q

Transfusions

A
  • A loss of blood greater than 30% (~2-3 liters) can cause severe shock; possibly fatal
  • Whole blood transfusions
  • Packed red cells (most of plasma removed), with heparin as the anticoagulant
64
Q

types of blood antigens

A

Glycoproteins (antigens) located on the surface of RBC’s
There are at least 30 different types of antigens

ex: ABO

65
Q

ABO blood groups

A

Based on presence or absence of two agglutinogens (A and B) on surface of RBCs
-Type A has only A agglutinogen
-Type B has only B agglutinogen
-Type AB has both A and B agglutinogens
-Type O has neither A nor B agglutinogens
Blood may contain preformed anti-A or anti-B antibodies
agglutinins)
Act against transfused RBCs with ABO antigens not present on recipient’s RBCs

66
Q

Rh blood groups

A
  • Rh+ indicates presence of D antigen
  • 85% of Americans are Rh+
  • Anti-Rh antibodies are not spontaneously formed in Rh negative individuals
  • Anti-Rh antibodies form if Rh- individual receives Rh+ blood, or Rh- mom is carrying Rh+ fetus
  • Second exposure to Rh+ blood will result in typical transfusion reaction
67
Q

Antigens promote

A

gglutination (clumping), and are termed agglutinogens

68
Q

In the plasma, there are preformed antibodies called agglutinins, which are

A

unreactive to a persons own red blood cells

69
Q

universal donor

universal recipients

A

donor: type o
recipient: type AB

70
Q

Autologous transfusions:

A

redonate blood for elective surgery, to avoid transfusion problems and/or disease transmission

71
Q

Examination of blood can yield information on persons health:
Low hematocrit
Blood glucose
Leukocytosis

A

Low hematocrit seen in cases of anemia
Blood glucose tests check for diabetes
Leukocytosis can signal infection

72
Q

Differential WBC count

A

looks at relative proportions of each WBC

Increases in specific WBC can help with diagnosis

73
Q

Prothrombin time and platelet counts

A

assess hemostasis

74
Q

CMP (comprehensive medical panel):

A

blood chemistry profile that checks various blood chemical levels
Abnormal results could indicate liver or kidney disorders

75
Q

Complete blood count (CBC)

A

checks formed elements, hematocrit, hemoglobin

A+P 2 (13 decks)

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