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HAN 202 > Chapter 17- Blood > Flashcards

Chapter 17- Blood Flashcards

1
Q

Functions of blood

A
  1. Distribution of:
    - > oxygen and nutrients to body cells
    - >metabolic wastes to the lungs and kidneys for elimination
    - > hormones from endocrine organs to target organs
  2. Regulation of:
    - >Body temperature (by absorbing and distributing heat
    - >maintain normal pH (7.35-7.45) using buffers
    - >adequate fluid volume in the circulatory system
  3. Protection against
    - >blood loss– plasma proteins and platelets initiate clot formation
    - > infection– antibodies, complement proteins, WBCs defend against foreign invaders
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2
Q

Functions of blood- distribution

A
  1. Distribution of:
    - > oxygen and nutrients to body cells
    - >metabolic wastes to the lungs and kidneys for elimination
    - > hormones from endocrine organs to target organs
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3
Q

Functions of blood- regulation

A
  1. Regulation of:
    - >Body temperature (by absorbing and distributing heat
    - >maintain normal pH (7.35-7.45) using buffers
    - >adequate fluid volume in the circulatory system
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4
Q

Functions of blood- protection

A
  1. Protection against
    - >blood loss– plasma proteins and platelets initiate clot formation
    - > infection– antibodies, complement proteins, WBCs defend against foreign invaders
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5
Q

Blood composition

A
  • > Fluid connective tissue composed of
  • plasma (55% of blood)

*formed elements (45% blood of blood)

*erythrocytes (red blood cells):
-Hematocrit:
percent of blood volume that is in RBCs. 47% plus/minus 5% for males. 42% plus/minus 5% for females

  • leukocytes (white blood cells)
  • platelets
  • > pH 7.35-7.45 (slightly basic)
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6
Q

hematocrit (Hct)

A

RBC/total blood volume

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7
Q

Formed elements when blood drawn and put into a centrifuge

A

Plasma:

  • 55% of whole blood
  • least dense component

Biffy coat:

  • leukocytes and platelets
  • <1% of whole blood

Erythrocytes:

  • 45% of whole blood
  • most dense component
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8
Q

Hematopoiesis

A

Hemopoiesis:

  • blood cell formation
  • occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur

Hemocytoblasts (hematopoietic stem cells):

  • give rise to all formed elements
  • hormones and growth factors push the cell toward specific pathway of blood cell development
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9
Q

Hemocytoblasts

A
  • > hematopoietic stem cells
  • > give rise to all formed elements
  • > hormones and growth factors push the cell toward a specific pathway of blood cell development
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10
Q

Erythropoiesis

A

-red blood cell production

hemocytoblast-> erythrocyte
takes 15 days. color changes from blue of ribosomes to pink of hemoglobin

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11
Q

Regulation of erythropoiesis

A
  • > too few RBCs leads to tissue hypoxia
  • > too many RBCs increases blood viscosity

balance between RBC production and destruction depends on:

  • hormonal controls
  • adequate supplies of iron, amino acids, and B vitamins
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12
Q

Hormonal control of erythropoiesis

A

Erythropoietin (EPO):

  • hormone that stimulates erythropoiesis
  • released by the kidneys in response to hypoxia

Effects of EPO:

  • increases production of RBCs
  • testosterone also enhances EPO production, resulting in higher RBC counts in males (Lance Armstrong scandal)

Dietary requirements:

  • Nutrients
  • iron
  • Vitamin B12
  • Folic acid
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13
Q

Erythropoietin (EPO)

A

Erythropoietin (EPO):

  • hormone that stimulates erythropoiesis (red blood cell production)
  • released by the kidneys in response to hypoxia
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14
Q

Effects of erythropoietin (EPO)

A

Effects of EPO:

  • increases production of RBCs
  • testosterone also enhances EPO production, resulting in higher RBC counts in males (Lance Armstrong scandal)
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15
Q

Negative feedback cycle

A

1 Stimulus:
-Hypoxia (low blood oxygen carrying ability) due to– decreased RBC count, decreased amount of hemoglobin, decreased availability of oxygen

2 Kidney (and liver to a smaller extent) releases erythropoietin

  1. Erythropoietin stimulates red bone marrow

4 enhanced erythropoiesis increases RBC count

5 Oxygen carrying ability of blood increases

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16
Q

Leukopoiesis

A
  • Production of white blood cells
  • stimulated by chemical messengers from bone marrow and mature WBCs
  • all leukocytes originate from hemocytoblasts
  • there are 5 main types of WBCs

(many of the hematopoietic hormones (EPO) are used with cancer or AIDS patients to stimulate bone marrow

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17
Q

Blood plasma (90-92% water)

A
  • > Plasma proteins- contribute to osmotic pressure, most common is albumin
  • > Nitrogenous by-products of metabolism- lactic acid, urea, and creatinine
  • > Nutrients- glucose, lipids, amino acids, vitamins
  • > electrolytes- Na+, K+Ca+, Mg+, Cl-, HCO3-…. most abundant
  • > respiratory gases- oxygens and CO2
  • > hormones
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18
Q

Formed elements

A

-> RBC, WBC, and platelets

  • > RBC majority of formed elements (99%)
  • RBCs have no nuclei or organelles
  • > only WBCs are complete cells
  • > platelets are cell fragments
  • > most blood cells originate in bone marrow and do not divide
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19
Q

Erythrocyte structure and function

A
  • > RBCs are dedicated to respiratory gas transport
  • biconcave discs, no nucleus, no organelles
  • > hemoglobin binds reversibly with oxygen
  • > iron atom in each heme can bind to one oxygen molecule
  • > Each hemoglobin can transport 4 oxygens
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20
Q

Life of a RBC

A
  • > Birth: red bone marrow. 15 days to grow
  • > lives for about 120 days
  • > dies in the SPLEEN, macrophages destroy old and damaged RBCs
  • > hemoglobin is broken down and parts are either recycled or excreted
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21
Q

Erythrocyte disorders

A
  1. Anemia:
    - low oxygen carrying capacity causes: blood loss, low RBCs produced, abnormal RBC
  2. Polycythemia: excess of RBC (increases viscosity)
    - > bone marrow cancer
    - >secondary polycythemia- when oxygen is available (high altitude) or when EPO production increases
    - >blood doping- causes increase risk of MI, stroke or blood clots
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22
Q

Anemia

A

-low oxygen carrying capacity causes: blood loss, low RBCs produced, abnormal RBC

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23
Q

Polycythemia

A

excess of RBC (increases viscosity)

  • > bone marrow cancer
  • > secondary polycythemia- when oxygen is available (high altitude) or when EPO production increases
  • > blood doping- causes increase risk of MI, stroke or blood clots
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24
Q

causes of anemia

A
  1. Blood loss- hemorrhagic anemia
  2. Not enough RBC produced:
    * Pernicious anemia: vitamin B12, intrinsic factor
    * Aplastic anemia: destruction of bone marrow by drugs
  3. RBC destroyed orr abnormal hemoglobin:
    * hemolytic anemia- mismatched blood
  • thalassemias- genetic disease of mediterranean ancestry
  • sickle cell anemia: abnormal hemoglobin
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25
Q

Leukocytes

A
  • > Make up less 1% of total blood volume
  • > can leave capillaries via diapedesis
  • > move through tissue spaces by ameboid motion and positive chemotaxis (follows trail released by damaged cells)
  • > leukocytosis: WBC count over 11,000 (normal response to bacterial or viral invasion)
26
Q

Granulocytes

A
  • > Granulocytes:
  • neutrophils
  • eosinophils
  • basophils
  • > cytoplasmic granules stain specifically with Wright’s stain
  • > larger and shorter-lived than RBCs
  • > lobed nuclei
  • > 1st stand during an infection, they attack in large numbers and eat until they die. “phagocytic”
  • > ex: pus in an infected wound are dead granulocytes
27
Q

Granulocytes

A
  • > Neutrophils:
  • bacteria slayers- phagocytic
  • most numerous
  • > eosinophils:
  • digest parasitic worms
  • elevated with allergies
  • phagocytic
  • > Basophils:
  • contain histamine
  • promotes inflammation
28
Q

Neutrophils

A
  • > Granulocyte
  • bacteria slayers- phagocytic
  • most numerous
29
Q

eosinophils

A
  • > granulocyte
  • digest parasitic worms
  • elevated with allergies
  • phagocytic
30
Q

Basophils

A
  • > granulocyte
  • contain histamine
  • promotes inflammation
31
Q

Agranulocytes (no granules)

A
  1. Lymphocytes
    * mostly in lymph tissue
    * crucial to immunity
    * T cells and B cells
  2. Monocytes
    * largest WBC
    * “big eaters” against viruses and bacteria
    * becomes macrophage when it leaves blood stream
32
Q

Lymphocytes

A

-> agranulocyte (no granules)

  • mostly in lymph tissue
  • crucial to immunity
  • T cells and B cells
33
Q

Monocytes

A

-> agranulocyte (no granules)

  • largest WBC
  • “big eaters” against viruses and bacteria
  • becomes macrophage when it leaves blood stream (in the tissues)
34
Q

Leukocyte disorders

A
  • > Leukopenia (penia=poverty)
  • abnormally low WBC count–drug induced (usually anti-cancer drugs)
  • > Leukemias
  • cancerous conditions involving overproduction of WBCs
  • WBCs are nonfunctional and cannot defend body
  • treatments include irradiation, antileukemic drugs (destroys the rapidly dividing cell), and stem cell transplants
35
Q

Leukopenia

A
  • > leukocyte disorder

* abnormally low WBC count–drug induced (usually anti-cancer drugs)

36
Q

Leukemias

A
  • > leukocyte disorder
  • cancerous conditions involving overproduction of WBCs
  • WBCs are nonfunctional and cannot defend body
  • treatments include irradiation, antileukemic drugs (destroys the rapidly dividing cell), and stem cell transplants
37
Q

Platelets

A
  • > Small fragments of megakaryocytes , not really cells
  • > formation is regulated by thrombopoietin (hormone)
  • > granules contain many chemicals that aide in clotting process
  • > forms a temporary plug in a broken blood vessel
38
Q

A. Hemostasis

A
  • fast series of reactions for stoppage of bleeding
  1. vascular spasm
  2. platelet plug formation
  3. coagulation (blood clotting)
39
Q
  1. Vascular spasm
A
  • this is the first step in hemostasis (stoppage of bleeding)
  • vasoconstriction of damaged blood vessel, constricted blood vessel reduces blood loss allowing time for the next 2 steps
  • triggers:
  • direct injury
  • chemicals released by endothelial cells and platelets
  • pain reflexes
40
Q
  1. platelet plug formation
A
  • this is the second step in hemostasis (stoppage of bleeding)
  • positive feedback cycle because as more platelets stick together, there is an increase in chemicals released and more platelets arrive
  • at site of blood vessel injury, platelets stick to exposed collagen fibers with the help of clotting factors (a plasma protein)
41
Q
  1. coagulation
A
  • this is the third step in hemostasis (stoppage of bleeding)
  • a set of reactions in which blood is transformed from a liquid to a gel
  • reinforces the platelet plug with fibrin threads, “molecular glue”
  • has 3 stages that use clotting factors made in the liver. clotting factors are numbered from I to XIII
42
Q

coagulation steps

A
  • 3 phases of coagulation:
    1. prothrombin activator is formed (intrinsic and extrinsic pathways)
    2. prothrombin is converted into thrombin
    3. thrombin catalyzes the joining of fibrinogen to form a fibrin mesh
  • starts with clotting factors and ends with fibrin mesh
43
Q

B. Clot retraction

A
  • actin and myosin in platelets contract within 30-60 min, draws ruptured edges of blood vessel more closely together
  • platelets pull on the fibrin strands, squeezing serum from the clot
44
Q

C. clot repair

A
  • platelet derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
  • growth factors stimulate endothelial cells to multiply and restore the endothelial lining
  • new cells grow to repair wound site
45
Q

D. fibrinolysis

A
  • begins within 2 days, removes unneeded clots
  • plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin
  • plasmin is a fibrin-digesting enzyme
46
Q

Clotting overview

A

A. Hemostasis: stops bleeding

B. clot retraction: draws edges of blood vessel together

C. clot repair: rebuild vessel wall

D. fibrinolysis: plasmin digests fibrin

47
Q

factors limiting clot growth or formation

A
  • > homeostatic mechanisms prevent clots from becoming large
  • swift removal and dilution of clotting factors (swift blood flow)

*inhibition of activated clotting factors
^ most thrombin is bound to fibrin threads, and prevented from acting elsewhere- fibrin acts as an anticoagulant (keeps thrombin local)

^heparin, another anticoagulant, also inhibits thrombin activity

***need to inhibit or inactivate thrombin

48
Q

factors preventing undesirable clotting

A
  • > platelet adhesion is prevented by:
  • smooth endothelial lining of blood vessels
  • antithrombic substances: nitric oxide and prostacyclin secreted by endothelial cells
  • vitamin E, which acts as a potent anticoagulant
49
Q

disorders of hemostasis: Thromboembolic

A
  • > Thromboembolic disorders: undesirable clot formation
  • Thrombus: stationary clot; DVT
  • embolus: travelling clot; PE (becomes an embolism if it wedges in a vessel)

Prevented by blood thinners (ant-coagulants)

50
Q

disorders of hemostasis: bleeding disorders

A
  • abnormalities that prevent normal clot formation
  • thrombocytopenia: decreased # of platelets
  • hemophilia: hereditary bleeding disorders
51
Q

Rh factor

A

type of protein on surface of RBC

-> 85% of people of Rh+

52
Q

ABO blood groups

A
  • > Types A, B, AB, and O
  • > Based on the presence or absence of two agglutinogens (A and B) on the surface of the RBCs
  • > Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present
  • > Anti-A or anti-B form in the blood at about 2months of age
53
Q

hemolytic disease of the newborn

A
  • > Also called erythroblastosis fetalis. Mother is Rh neg and father is Rh +, baby will be Rh+
  • > Rh– mother becomes sensitized when exposure to Rh+ blood during delivery & produces anti-Rh antibodies
  • > During 2nd pregnancy, antibodies cross the placenta and destroy the RBCs of an Rh+ baby
54
Q

tranfusion reactions

A
  • occur if mismatched blood is infused

Donor’s cells:
-Are attacked by the recipient’s plasma agglutinins (antibodies)

  • Agglutinate and clog small vessels
  • Rupture and release free hemoglobin into the bloodstream
  • Symptoms: skin flushing, fever, pain
  • > Result in:
  • Diminished oxygen-carrying capacity

-Hemoglobin in kidney tubules and renal failure

55
Q

Restoring blood volume

A

-> Death from shock may result from low blood volume

  • > Volume must be replaced immediately with:
  • Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition
  • Plasma expanders
  • -Mimic osmotic properties of albumin (pulls water in)
  • -More expensive and may cause significant complications
56
Q

Hematocrit

A

oxygenation status

57
Q

blood glucose tests

A

metabolic function, increased levels in diabetes

58
Q

differential WBC count

A

increased with infections

59
Q

prothrombin time and platelet counts assess hemostasis- clotting mechanisms

A

yes

60
Q

SMAC

A

a blood chemistry profile (sequential multiple analysis with computer)

61
Q

complete blood count (CBC)

A

counts of different formed elements, hematocrit, hemoglobin content and size of RBC

HAN 202 (13 decks)

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