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Anatomy II > Chapter 17- Blood > Flashcards

Chapter 17- Blood Flashcards

1
Q

Blood Functions

A
  1. Transport
  2. Maintenance
  3. Protection
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2
Q

Transport Blood Function

A

Oxygen and nutrient delivery to tissues
Waste removal from tissues
(nitrogenous and carbon dioxide)
Hormone transport to target organs

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3
Q

Maintenance blood function

A

Body temperature (blood is mostly water and water absorbs heat and maintains 98.6)
pH (all chem reactions take place with a limited set of pH volumes)
Fluid volume (blood pressure and circulation)

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4
Q

Characteristics of Blood

A

Scarlet to dark red in color
pH Range- 7.35-7.45
Viscous (thickness) due to erythrocytes (red blood cells)

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5
Q

What causes the color difference in blood?

A

Oxygen content of the blood
Red blood cells have hemoglobin that binds and carries oxygen (causes redness)

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6
Q

Blood Composition

A

Blood Plasma
Blood Cells

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7
Q

Blood Plasma

A

The fluid portion of blood (non-living)
90% water
6 solutes found in plasma
(Electrolytes, nitrogenous substances, organic nutrients, respiratory gasses, hormones, plasma proteins)

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8
Q

Electrolytes

A

Found in plasma
Most numerous

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9
Q

Nitrogenous substances

A

Found in plasma
Urea, uric acid

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10
Q

Organic nutrients

A

Found in plasma
Glucose, amino acids, triglycerides, tc.

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11
Q

Respiratory gasses

A

CO2 found more here than in erythrocytes

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12
Q

Hormones

A

Found in plasma

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13
Q

Plasma Proteins

A

Make up most of the mass of the plasma
Mostly produced by liver
Serve as carrier/transport protein that bind to another substance and allow it to move through the blood to used by cells for energy or nutrients

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14
Q

Albumin

A

Type of plasma protein
Prevents water from leaving the bloodstream
Major transport protein of blood and contributes to osmotic pressure (water moving into a more concentrated substance) in capillaries
Found in blood vessel stream and because it is so large in size, water will be pulled towards it

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15
Q

What would happen to water in the blood plasma if albumin were absent?

A

If absent, water would leave the bloodstream
BP would tank
If water enters all body tissues, you would flood the tissue with water and can impair their function

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16
Q

What would happen to water in the blood plasma if albumin were absent?

A

If absent, water would leave the bloodstream
BP would tank
If water enters all body tissues, you would flood the tissue with water, and can impair their function

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17
Q

Blood Cells

A

Short-lived (at MOST, 4 months, some 5-10 days)
Non-mitotic (will not divide)
Built-in mechanism to produce more of these blood cells for the lifetime

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18
Q

Erythrocytes

A

Red blood cells
Respiratory gas transport
Hematocrit

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19
Q

Hematocrit

A

Portion of total blood volume made up by erythrocytes
Males- around 47%
Females- around 42%
showing a small influence of testosterone on red blood cell hematocrit

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20
Q

Leukocytes

A

White blood cells
Protection/infection

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21
Q

Thrombocyte

A

Platelets
Blood clotting/preventing blood loss

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22
Q

Hematopoiesis

A

Production of blood cells
Occurs in red bone marrow (kids- RBM everywhere but adults- RBM only in certain bones)
All blood cells come from hematopoietic stem cell
In a single day, marrow creates around 100 billion new cells

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23
Q

Hematopoietic stem cell

A

Become committed to forming a certain type of blood cell
Once committed, the cell cannot become another type of cell

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24
Q

Erythrocytes (expanded)

A

Blood cell type responsible for respiratory gas transport
Nuclei and organelles removed during cell development for more ability to carry oxygen through hemoglobin

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25
Q

What is the advantage to having no nuclei or organelles?

A

Creating more space for hemoglobin which increases oxygen carrying capacity

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26
Q

Hemoglobin

A

Protein responsible for O2 transport in blood (molecule)
composed of heme pigment bound to globin protein

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27
Q

Globin Protein

A

2 alpha chains, 2 beta chains
Each chain binds to 1 heme group

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28
Q

Heme Group

A

Fe+ ion at center
Fe+ can bind one molecule O2
4 O2’s can bind to a single hemoglobin

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29
Q

Hemoglobin binds and breaks from oxygen very easily

A

Important- so we can take in as much oxygen as we can for all our body tissues
Will be unloaded very easily so our tissue cells have access
If it was more difficult, it would have lower than normal oxygen levels

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30
Q

Other features that make erythrocytes ideal for gas exchange

A
  1. Large surface area relative to volume (increased surface area = increased diffusion rate of O2)
  2. Flattened disc-shape (Flat shape = increased diffusion rate of O2)
  3. Anaerobic mechanism of energy production (RBC don’t use any of the oxygen that thy carry, maximizes O2 to tissue cells)
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31
Q

Erythropoiesis

A

The production of red blood cells
Hematopoietic stem cell “commits” to a proerythroblast
Tightly regulated process to keep the balance

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32
Q

Hypoxia

A

Too few erythrocytes
Not enough hemoglobin to reach the body tissues
Lead to cell and tissue death, can be reversed as long as you can get oxygen there

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33
Q

Too many erythrocytes

A

too viscous and slow down oxygen delivery in the blood vessels

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34
Q

Hormonal Controls of erythropoiesis

A

Erythropoietin
Testosterone

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35
Q

Erythropoietin

A

Hormone control
Stimulates erythrocyte production
Small amounts almost always present in the blood to set the basal rate of production

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36
Q

What causes an increase in EPO release?

A

Negative feedback mechanism- Excessive oxygen supply

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37
Q

Testosterone

A

Enhances the production of EPO
Males generally have more erythrocytes and Hemoglobin than females

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38
Q

Dietary needs for normal erythrocyte production

A

General nutrients
B-complex vitamins
Iron

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39
Q

General Nutrients for normal erythrocyte production

A

Amino acids
Lipids
carbohydrates for cell synthesis

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40
Q

B complex vitamins

A

B12 and folic acid (B9)
Necessary for normal DNA synthesis
Red blood cells can get rid of nucleus and DNA but before that it will direct normal cellular development

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41
Q

Iron

A

Normal Hb synthesis
65% of body’s iron supply is in Hb
Other 35% remains stores in the liver, spleen, etc.
“Free” iron bound to protein transferrin (erythrocyte takes up iron as needed)

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42
Q

Transferrin

A

Toxic and can impair normal cellular function in the body

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43
Q

Detroying Erythrocytes

A

Average lifespan- 120 daysish
Hb begins to degenerate, cell becomes less flexible and can’t go to many places
Macrophages engulf and destroy cell where
1. heme group splits from globin and
2. Iron bound to transport protein and saves for reuse in the liver

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44
Q

Bilirubin

A

Heme group broken down into this in the liver and go to the intestines in bile –> feces
Globin is broken down into amino acids and released to circulation

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45
Q

Anemia

A

Insufficient oxygen supply to meet body needs
Symptoms- Paleness, cold, short-of-breath, third
Causes hypoxis and and indicator of a larger problem

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46
Q

Anemia is caused by…

A
  1. Blood loss
  2. Inadequate erythrocyte production
  3. Excessive erythrocyte destruction/deformation
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47
Q

Acute hemorrhagic anemia

A

Severe, sqift blood loss

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48
Q

Chronic Hemorrhagic anemia

A

Slow, persistent blood loss (ulcer bleeding, hemorrhoids)

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49
Q

Inadequate erythrocyte production example

A

iron-deficiency anemia
(nutritional origins), renal anemia (little/no EPO release - kidneys)

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50
Q

Excessive erythrocyte destruction/deformation example

A

Sickle Cell Anemia (beta chains deformed and don’t bind as readily and will have hooks that will make RBC’s clump together and inhibit blood circulation)

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51
Q

Polycythemia

A

Increase in the number of erythrocytes
Causes too many red blood cells and increases blood viscosity and thickness

52
Q

Polycythemia vera

A

Bone marrow cancer
Hematocrit levels - around 80%
Huge increase in red blood cells and much more thick blood
Effect- blood volume doubles, vascular system engorges with blood and impairs circulation
treatment- therapeutic phlebotomy (drawing blood)

53
Q

Secondary polycythemia

A

Increased EPO release, low oxygen availability
Caused by- High altitude living
Response- increase amount of red blood cells

54
Q

Blood Doping

A

Boost red blood cell numbers by boosting the amount of oxygen that gets in lung tissue
Blood is removed and the body will replace the blood it lost and put the blood back in to increase the oxygen amount before competing
Used by athletes
(temporary polycythemia- synthetic EPO/oxygen carriers, blood transfusions)
Risks- hemorrhagic stroke, heart failure

55
Q

Leukocytes

A

White blood cells
Responsible for defending the body
Characteristics…
1. Not restricted to blood vessels (can go to dif parts of the body through capillary walls and can directly encounter the infectious areas right at the sight of injury)
2. Can be produced very quickly (Number in the body can double within 2-3 hours, can kill off the microorganisms on the spot and don’t want so many, creates tons of them for a small number of microorganisms until it becomes a threat)
3. Average lifespan- 13-20 days

56
Q

Granulocytes

A

White blood cells that help with defense
Spherical in shape, large, and packed with granules

57
Q

Types of granulocytes

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
58
Q

Neutrophils

A

Bacteria killer
50-70% of leukocyte population
contain defensins
chemically attracted to sites of inflammation
Can be phagocytic

59
Q

Defensins

A

Antimicrobial protein
Kill off bacteria by punching holes in membrane of the bacteria
Will fill with water according to the concentration gradient (low to high solute)

60
Q

Eosinophils

A

Parasite killer
2-4% leukocyte population
Break down the body wall of a parasitic worm
Lysosomes in cell contain digestive enzymes
If fail- results in tapeworms

61
Q

Basophils

A

.5-1% leukocyte population
Histamine-containing granules (release causes vasodilation and attracts more WBC/blood flow to that area)
Chemical attractant
Example- Allergies; basophils overreact to pollen and release histamine

62
Q

Agranulocytes

A

Leukocytes that lack visible granules
1. Lymphocytes
2. Monocytes

63
Q

Lymphocytes

A

25% Leukocyte population
Found in lymphoid tissue (lymphatic system)
Types…
1. T-lymphocytes (t-cells) –> Act against virus-infected cells and tumor cells (Immune function outside the body and internally that prevents cancerous/tumor growth before it becomes a problem)
2. B-lymphocytes (b-cells) –> Produce antibodies released to blood (red flag that is responsible for tagging infected cells)

64
Q

Monocytes

A

3-8% leukocyte population
Differentiate into macrophages as they leave the bloodstream and enter tissue
Phagocytic and destroy bacteria, viruses, sources of chronic infection, destroy anything

65
Q

Leukopoiesis

A

Production of leukocytes
Stimulated by…
1. interleukins
2. colony-stimulating factors

66
Q

Leukocyte differentiation

A

Hematopoietic stem cell can form either…
1. Myeloid stem cell –> myeloblast or monoblast
2. Lymphoid stem cell –> commits to B or T-lymphocyte precursor cells

67
Q

Leukemia

A

Cancer resulting in over-production of abnormal leukocytes
WBC’s must be taught what they are defending against
“Extra” cells originate from a single abnormal cell - remain unspecialized, proliferate extensively

68
Q

What does it mean when you say abnormal WBCs proliferate extensively?

A

Cancerous leukocytes crowd the red bone marrow and immature leukocytes flood the bloodstream
Other blood cell types are crowded out of blood, resulting in anemia and bleeding problems
Lower oxygen-carrying capacity
Don’t defend the body as they should and cause infection and hemorrhage

69
Q

Acute leukemia

A

Derived from stem cells
Primarily affect children
Development is quick

70
Q

Chronic Leukemia

A

Derived from later cell stages
Primarily affect the elderly
Development more slow

71
Q

Myeloid leukemia

A

Involved myeoloid stem cell descendants

72
Q

Lymphocyte leukemia

A

Involves lymphocytes

73
Q

Infectious mononucleosis

A

“kissing disease”
Epstain-Barr Virus
high number of WBC and look like a monocyte
Symptoms- low grade fever, fatigue, body soreness, sore throat
No treatment

74
Q

Thrombocytes (expanded)

A

Blood platelets
Fragments of large cells called megakaryocytes
Average lifespan- 10 days if unused
Function- INitiate blood clot formation after damage to the blood vessel wall

75
Q

What happens when the blood vessel wall is damaged/torn?

A

Platelets stick to each other and to the injury site and could clump together (catastrophe)

76
Q

What happens when the blood vessel wall is not damaged/torn?

A

Prostacyclin and nitric oxide stop the platelets from sticking together

77
Q

What is platelet formation regulated by?

A

Thrombopoietin- released by liver cells (and a but from kidneys and bone marrow)

78
Q

Hemostasis

A

The process by which bleeding is stopped after blood vessel rupture occurs
Localized response that progresses very quickly

79
Q

Vacular spasm

A

Raid constriction of an injured blood vessel
Triggered by…
1. Injured smooth muscle tissue
2. Chemicals released by damaged endothelial cells of vessel wall
3. Reflexes from local pain receptors

80
Q

What is the immediate benefit of the vascular spasm?

A

Smaller blood vessels can’t hold as much as blood as larger ones
Letting loose blood into it automatically decreasing blood loss before you begin using platelets
Decreases blood flow to a damaged area

81
Q

Platelet Plug Formation

A

Platelets stick to each other and to fibers in blood vessel wall to form a plug in a damaged blood vessel
Constrict on its own
Good for general wear and tear and small injuries
Larger injuries require more severe mechanisms

82
Q

What do platelets release in response to injury?

A
  1. ADP (causes more platelets to stick to the site of injury)
  2. Serotonin, thromboxane A2 (Increase vascular spasm and platelet aggregation)
83
Q

Larger injuries require more severe mechanisms to stop bleeding

A

True blood clot formation
Structurally and physiologically blood clots are much more complex than platelet plugs

84
Q

Coagulation

A

Formation of a blood clot

85
Q

Process of coagulation

A
  1. Severe clotting factors 13 involved to form prothrombin activator
  2. Prothrombin activator catalyzes the conversion of plasma protein prothrombin into active enzyme thrombin
  3. Thrombin catalyzes transformation of soluble clotting factor fibrinogen into fibrin molecules (insoluble form)
    Trap platelets and form a blood clot and anything that tries to pass through get trapped in a clot
86
Q

Factor 13

A

Enzyme that binds fibrin strands to one another

87
Q

Why is it important to bind fibrin strands to one another

A

To strengthen the blood clot
The more they are connected, the stronger the clot will be

88
Q

Why is it important to bind fibrin strands to one another

A

To strengthen the blood clot
The more they are connected, the stronger the clot will be

89
Q

Blood Clot Retraction

A

The process of pulling damaged edges of blood vessel close together (have to replace the damaged tissue)
Platelets in blood clot have contractile ability to seal off the wound

90
Q

Platelet-derived growth factor

A

Causes increase in number of fibroblasts and smooth muscle cells in damaged area
Forms connective tissue that will eventually form new blood vessel wall where damage occurred
Drives the repair of the blood vessel wall

91
Q

Fibrinolysis

A

The removal of blood clot after healing is complete through plasmin
Begins within 2 days of clot formation

92
Q

Why is fibrinolysis necessary after healing is complete?

A

Because you can suffer damage to the same blood vessel in the same area multiple times in your life - if they don’t repair, blood clots would form on top of each other and it would cause blood vessel blockage; by destroying the blood clots, you free up space for the blood vessels

93
Q

Plasmin

A

Enzyme that digests fibrin

94
Q

Thromboembolic disorders

A

Formation of undesired/unnecessary blood clots

95
Q

Thrombus

A

Formation of blood clot in unbroken vessel (remains stuck to vessel wall)
Effect- Blocks circulation
How much it slows down depends on how large the thrombus is

96
Q

Embolus

A

Thrombus that enters circulation
Effect-
1. if small- Not a problem
2. If big- can obstruct smaller blood vessels and block circulation
leads to cerebral stroke or pulmonary embolism

97
Q

Bleeding Disorders

A

Absence of desirable blood clots, leading to excessive bleeding

98
Q

Thrombocytopenia

A

Low number of platelets in circulation
Limited ability to form platelet plugs - even small breaks can cause huge hemorrhage
Caused by- anything that decreases RBM decreases platelet count

99
Q

Hemophilia

A

Hereditary bleeding disorder
Blood loving
Deficiency or absence of certain clotting factors causes extreme bleeding from small cuts/injuries
Fibrin strands are not being produced or too low that they aren’t affective
Symptoms- Prolonged bleeding into tissues, painful/disabled joints

100
Q

Hemophilia A

A

Deficiency of clotting factor 8

101
Q

Hemophilia B

A

Deficiency of clotting factor 9

102
Q

Hemophilia C

A

Lack of factor 11

103
Q

Why are males more likely to have hemophilia?

A

Found on the X chromosome

104
Q

Treatment for hemophilia

A

Plasma transfusions
Injections of absent/deficient clotting factor
insanely expensive

105
Q

Blood transfusions

A

Body compensates for blood loss in 2 ways
1. Decreasing blood volume to injured blood vessels
2. Increasing RBC production by red bone marrow

106
Q

Why do we increase RBC?

A

Increase erythropoietin = losing blood cells loses the ability to oxygenate body tissues and don’t risk them dying off
Can only build clots that are so large - if they are large/deep injuries, you can’t compensate as much

107
Q

The body can only compensate so much

A

Losing 15-30% total blood volume leads to weakness, 30%+ loss leads to severe shock (possibly death)

108
Q

Whole blood transfusions are rare

A

Only necessary when large volumes of blood are lost
More often, red cell transfusions are used - giving individuals the oxygen they need to be kept alive
Immediate threats- hypoxia and tissue death

109
Q

Antigens

A

Erythrocytes have very specific extracellular markers
Transfusions between two people with different antigens usually cannoy occur
Immune system will attack “mismatched” blood cells

110
Q

ABO Blood groups

A

Blood type A: cells have “A” antigen
Blood type B: cells have “B” antigen
Blood type O: cells do not have any antigen
Blood type AB: cells have both ”A” and “B” antigen

111
Q

Agglutinins

A

immune system antibodies that will attack mismatched blood cells

112
Q

A person with Type A blood has what agglutinins

A

Anti-B agglutinins

113
Q

A person who Type B has what agglutinins

A

Anti-A agglutinins

114
Q

Person with Type AB blood has what antibody?

A

Neither type

115
Q

A person who Type O has what antibodies?

A

anti-A and anti-B antibodies

116
Q

Rh Blood Groups

A

Five antigens make up this blood group → C, D, E, c, and e

117
Q

Rh+

A

If you carry the D antigen

118
Q

Rh-

A

If you carry the C, E, c, or e antigen

119
Q

What are the “rules” for Rh +/- donation?

A
  1. Rh (-) will create antibodies IF mismatched
  2. rH (+) does NOT have any type of immune reaction if it is mismatched
120
Q

Can an rH - person donate blood to an rH + person?

A

Yes

121
Q

Can an rH + person donate blood to an rH - person?

A

No, can only receive negative

122
Q

Transfusion reaction

A

Mismatching blood types lead to this
Agglutinins attack “foreign” donor blood cells

123
Q

Agglutination

A

Foreign erythrocytes are clumped together through this
Blocking blood vessels
Blood cells will start to lyse - release hemoglobin to blood stream (clumping)

124
Q

Type O

A

Universal donor
Has both types of agglutinins
Almost 50 of the population has this

125
Q

If a person has type O blood, what other ABO blood groups can they receive blood from?

A

Only O

126
Q

Type AB

A

Universal recipient
Neither antibody is present
Least common blood type

127
Q

If a person has type AB blood, what other ABO blood groups can they receive blood from?

A

Anyone

Anatomy II (4 decks)

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