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Bio Exam 1: Blood > Blood > Flashcards

Blood Flashcards

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1
Q

Functions of the blood?

A
  • Oxygen from lungs to organs/cells
  • Carbon dioxide from cells to lungs
  • Nutrients from digestive system and storage
  • Wastes to liver and kidneys (metabolic reactions)
  • Hormones
  • Regulates body temperature (transports heat out of skin)
  • Immunity (WBC fight off infections)
  • Clotting (platelets)
  • Stabilizes water balance
  • Stabilizes pH (buffer for acids and bases)
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2
Q

What are the formed elements?

A

RBC, WBC, and platelets

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3
Q

What is an Erythocyte?

A

Red blood cell

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4
Q

What is a Leukocyte?

A

White blood cell

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5
Q

How many liters of blood do adults have?

A

4-6L

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6
Q

What is Plasma?

A

A clear extracellular fluid (55% of blood)

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7
Q

What is the mean erythrocyte count?

A

4.2-6.2 million/ml

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8
Q

What is the mean leukocyte count?

A

5,000-10,000/ml

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9
Q

What is the mean platelet count?

A

130,000-400,000/ml

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10
Q

What is a Granulocyte?

A
  • Little “grains of sand” in cells.
  • Neutrophils, Eosinophils, Basophils
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11
Q

What is an Agranulocyte?

A
  • No cytoplasmic granules
  • Lymphocytes and Monocytes (Macrophages)
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12
Q

What is Hematocrit?

A
  • the % of total volume that is cells.
  • Centrifuging blood forces formed elements to separate from plasma
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13
Q

How much total volume of hematocrit are in erythrocytes?

A
  • 37%-52% total volume
  • Erythrocytes are heaviest and settle first
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14
Q

How much hematocrit are in Leukocytes and platelets?

A
  • 1% total volume
  • Buffy coat
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15
Q

How much hematocrit is in plasma?

A

47%-63%

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16
Q

What is viscosity?

A
  • the resistance to flow (thickness/stickyness)
  • Blood is 4.5-5.5 times more viscous than water
  • Plasma alone is 2 times more viscous than water.
  • Too many or too few red blood cells changes the viscosity of blood and puts a strain on the heart
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17
Q

What is osmolarity?

A
  • total molar concentration of dissolved particles in 1L of solution due to transfer of nutrients and wastes between the blood and tissue fluids
  • more solute= more osmolarity
  • less solute= less osmolarity
  • it too high: bloodstream absorbs too much fluid from the tissues, thus causing hypertension (high BP)
  • if too low: bloodstream transfers too much fluid to tissues, resulting in edema and hypotension (low BP)
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18
Q

What does Plasma contain?

A
  • 92% water
  • proteins, enzymes, nutrients, wastes, hormones, lipids, trace elements, gases
  • serum: plasma minus the clotting proteins
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19
Q

True or False: Proteins are the most abundant solute in plasma?

A

True: they are used for clotting, defense, and transport

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20
Q

What are Albumins?

A
  • most abundant plasma protein
  • produced by the liver
  • contribute to viscosity and osmolarity and influences blood pressure, flow, and fluid balance.
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21
Q

What is Fibrinogen?

A

clotting protein

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22
Q

What are Globulins?

A

immune system defenses

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23
Q

What is Hemopoiesis?

A
  • Blood cell production: produce formed elements
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24
Q

What is red bone marrow?

A
  • produces RBCs, WBCs, and platelets
  • committed cells are destined to continue down a specific cell line
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25
Q

What are Hemopoietic stem cells?

A
  • adult stem cells that multiply continually and are pluripotent (capable of differentiating into multiple cell lines)
  • differentiate into colony-forming units (CFUs) that give rise to the different formed elements.
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26
Q

What is Erythropoietin?

A
  • hormone produced by the liver
  • no nucleus or organelles (does not undergo mitosis)
  • lives for ~120 days
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27
Q

What is Erythropoiesis?

A
  • the production of erythrocytes begins with a hemopoietic stem cell in the red bone marrow
  • Erythropoiesis produces 2.5 million RBCs/second
  • Development takes 3-5 days
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28
Q

What are the steps of Erythropoiesis?

A
  1. Hemopoietic stem cell
  2. Colony-forming unit (Erythrocyte CFU is present)
  3. Precursor cells (Erythroblasts and Reticulocytes are present)
  4. Mature cell (Erythrocyte is formed)
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29
Q

What are nutritional needs for Eythropoiesis?

A
  • iron, B12 and folic acid, Vitamin C and copper
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30
Q

Why is iron a nutritional need to erythropoiesis?

A
  • it is lost daily through urine, feces, and bleeding
  • low absorption rate requires consumption of 5-20mg/day
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31
Q

Why is B12 and folic acid a nutritional need for Erythropoiesis?

A
  • for DNA synthesis and rapid cell division
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32
Q

Why is Vitamin C and copper a nutritional need for Erythropoiesis?

A
  • Cofactors for enzymes synthesizing RBCs
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33
Q

Erythrocytes

A
  • disc-shaped, thick rim, sunken center
  • outer surface of the plasma membrane has glycoproteins and glycolipids
  • inner surface of plasma membrane has two types of proteins, actin and spectin (resilience and durability)
  • only cells of body that carry on anaerobic fermentation indefinitely, so they don’t use the O2n they transport
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34
Q

Major functions of Erythrocytes

A
  • gas transport!
  • increased surface area/volume ratio due to loss of organelles during maturation
  • ## 33% of cytoplasm is hemoglobin
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35
Q

What is carbonic anhydrase?

A
  • in cytoplasm
  • produces carbonic acid from CO2 and water
  • important role in CO2 gas transport and pH balance
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36
Q

How many protein chains does hemoglobin consists of?

A
  • 4 protein chains called globins
  • 2 alpha and 2 beta
  • each protein chain is conjugated with a heme group that binds oxygen to ferrous ion
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37
Q

How many oxygen can a hemoglobin molecule carry?

A

4 O2

38
Q

True of False: RBC count and hemoglobin concentration indicate the amount of oxygen the blood can carry.

A

True

39
Q

Why are the values of Erythrocytes and Hemoglobin lower in women?

A
  • lower hematocrit
  • androgens stimulate RBC production
  • women have periodic menstrual losses
  • counts are inversely proportional to body fat
40
Q

True or False: Women clot faster than men

A

False: Men’s blood clots faster because they have fewer skin blood vessels.

41
Q

What feedback control does Erythrocyte Homeostasis have?

A

Classical negative feedback control

42
Q

What is hypoxemia?

A
  • too few RBCs to supply body tissues with required amounts of O2= O2 deficiency
  • kidneys release erythropoietin: stimulate red bone marrow hemopoetic stem cells to differentiate into erythrocyte colony-forming units
43
Q

Negative feedback in erythrocyte homeostasis

A
  • as RBC counts rise, secretion of erythropoietin decreases
44
Q

What are the causes of hypoxemia?

A
  • loss of blood (bleeding, donating blood)
  • high altitudes: less O2 availability causes hypoxemia in the average individual with 5 million RBCs/ml
  • sedentary person starts exercise program, thus requiring more O2
45
Q

Erythrocyte death and disposal

A
  • RBCs live for ~120 days: membrane becomes fragile, deterioration of actin and spectrin. spleen is known as the erythrocyte graveyard
  • macrophages in spleen: digest membrane bits, separate heme from globin, hydrolyze globin–> amino acids, remove iron from heme, convert heme to bilirubin
46
Q

What is polycythemia?

A
  • an excess of RBCs
  • primary polycythemia: due to cancer of erythropoietic cell line (RBC count as high as 11 million; hematocrit of 80%
  • secondary polycythemia: RBC count up to 8 million
47
Q

More erythrocyte disorders…

A
  • dehydration: more RBCs due to less plasma
  • high altitude: edtended stay at high altitude. RBC rises to 7-8 million
  • physical conditioning: endurance trained athletes (higher RBC) have ~6.5 million RBCs due to higher oxygen requirements
    emphysema: less lung tissue. RBCs can’t correct for this, but erythropoietin is still released
48
Q

What are the dangers of polycythemia?

A
  • increased blood volume, pressure and viscosity can lead to poor circulation, heart strain and clogged capillaries (which can lead to embolism (traveling blood clots), stroke, or heart failure)
49
Q

What is iron-deficiency anemia?

A
  • dietary iron deficiency= Hb
  • not enough RBC
50
Q

What is Pernicious anemia?

A
  • inadequate vitamin B12
  • poor nutrition
  • lack of intrinsic factor (facilitates B12 absorption)
51
Q

What is Hypoplastic anemia?

A
  • decline in RBC production
  • kidney failure: insufficient erythropoietin hormone production
  • destruction of myeloid tissue
  • radiation, viral infection, poisoning, autoimmune disease
52
Q

What is aplastic anemia?

A
  • complete cessation of RBC production
  • cause is unknown
53
Q

What is Hemorhagic anemia?

A
  • loss of blood
54
Q

What is hemolytic anemia?

A
  • RBC destruction
  • motther-fetus mismatch, mushroom toxins, snake or spider venom, drug reactions, malaria (parasites destroy RBCs)
55
Q

What are the consequences of anemia?

A
  • tissues are deprived of O2 (hypoxia/hypoxemia)
  • shortness of breath
  • lethargy (lack of energy)
  • tissue necrosis (tissue destruction)
  • reduced blood viscosity: less blood flow resistance
    -heart beats faster
  • blood pressure drops
  • heart failure
56
Q

What is sickle-cell disease?

A
  • hereditary hemoglobin defects
  • caused by a recessive allele that modifies that structure of the hemoglobin molecule (HbS- hemoglobin S “sickle”)
  • Differs only on the sixth amino acids of the beta chain
  • HbS does not bing oxygen well
  • RBCs become rigid, sticky, pointed
  • Clump together and block small blood vessels causing intense pain
  • Can lead to kidney or heart failure, stroke, rheumatism, or paralysis
  • HbS is indigestible to malaria parasites so gene persists despite its harmful effects to the homozygous effects to the homozygous individuals.
57
Q

What are the abnormalities of Leukocyte count?

A
  • Leukopenia, leukocytosis, and leukemia
58
Q

What is Leukopenia?

A
  • low WBC count (<5000)
  • causes: radiation, poisons, infectious disease
  • effects: elevated risk of infection
59
Q

What is Leukocytosis?

A
  • high WBC count (>10,000)
  • causes: infection, allergy and disease
  • differential count distinguishes % of each cell type
60
Q

What is Leukemia?

A
  • cancer of hemopoietic tissue
  • myeloid and lymphoid: uncontrolled WBC production
  • acute or chronic (very fast) : death in either months or years
  • effects: normal cell % disrupted, patient subject to opportunistic infection, anemia and impaired clotting.
61
Q

What are Platelets?

A
  • small fragments of megakaryocytes (produced in bone marrow)
  • normal platelet count (130,000-400,000)
  • contribute less than WBCs to blood volume
62
Q

What is thrombopoiesis?

A
  • production of platelets
  • thrombo= clotting
  • contain “granules” and organells
  • amoeboid (pseudopod) movement and phagocytosis
63
Q

What are platelet functions?

A
  • secrete
  • clotting factos
  • growth factors for endothelial repair
  • vasoconstrictors in broken vessels
  • form temporary platelet plugs
  • dissolve old blood clots
  • phagocytize bacteria
  • attract WBCs to sites of inflammation
64
Q

Steps of Hemostasis: The control of bleeding

A
  1. Vascular spasm
  2. Platelet plug formation
  3. Blood clotting
    - effecting at closing breaks in small vessels
    - 3 hemostatic mechanisms: all involve platelets.
65
Q

What is vascular spasm?

A
  • prompt constriction of a broken vessel
  • most immediate protection against blood loss
66
Q

What are the causes of vascular spasm?

A
  • pain receptors: some directly innervate blood vessels to constrict (vasoconstriction)
  • smooth muscle injury: constrict when hurt
  • platelets release serotonin (vasoconstrictor)
67
Q

What are the effects of vascular spasm?

A
  • constriction of a broken vessel
  • pain receptors: short duration (minutes)
  • smooth muscle injury: longer duration
  • provides time for other two clotting pathways
68
Q

True or False: Endothelium is very smooth because it is coated with prostacyclin (a platelet repellant)

A

True

69
Q

What is the hemostasis platelet plug formation?

A
  • broken vessel exposes collagen
  • platelets; pseudopods stick to damaged vessel and other platelets; pseudopods contract and draw walls of vessel together forming a platelet plug
  • Platelets degranulate releasing a variety of substances (serotonin is a vasoconstrictor, ADP attracts and degranulates more platelets, Thromboxane A2 promotes platelet aggregation, degranulation, and vasoconstriction.
  • positive feedback cycle (until break in vessel is sealed)
70
Q

What is coagulation?

A
  • Clotting; last and most effective defense against bleeding
  • conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot
71
Q

What are Procoagulants?

A
  • Clotting factos; usually produced by the liver; are present in plasma at all times
  • activate one factor and it will activate the next to form a reaction cascade
72
Q

What is the extrinsic pathway?

A
  • factors released by damaged tissues begin cascade
  • initiated by release of tissue thromboplastin from damaged tissue
  • calcium is required for pathway
73
Q

What are the intrinsic pathways?

A
  • factors found in blood begin cascade (platelet degranulation)
  • initiated by platelets releasing Hagemen factor.
  • calcium required for pathway
74
Q

What is rapid clotting?

A
  • each activated cofactor activates many more molecules in next step of sequence
75
Q

What does the activation of factor X do?

A
  • leads to production of prothrombin activator
76
Q

What does the Prothrombin activator do?

A
  • converts prothrombin to thrombin
77
Q

What does thrombin do?

A
  • converts fibrinogen into fibrin
  • positive feedback: thrombin speeds up formation of prothrombin activator.
78
Q

What is a platelet-derived growth factor?

A
  • secreted by platelets and endothelial cells (facilitate healing)
  • mitotic stimulant for fibroblasts and smooth muscle to multiply and repair the damaged vessel
79
Q

What is fibrinolysis?

A
  • dissolution of clot
  • plasminogen (inactive protein) converted into plasmin (a fibrin- dissolving enzyme or clot bust
80
Q

What is platelet repulsion?

A
  • platelets do not adhere to prostacyclin-coating
81
Q

What is thrombin dilution?

A
  • activates clotting cascade
  • normally diluted by rapidly flowing blood
  • heart slowing in shock can result in clot formation
82
Q

What is a natural anticoagulant?

A
  • antithrombin produced by the liver deactivates thrombin before it can act on fibrinogen
83
Q

What is heparin?

A
  • secreted by basophils and mast cells interferes with formation of prothrombin activator
84
Q

What disorders have insufficient clotting?

A
  • thrombocytopenia and hemophilia
85
Q

What is thrombocytopenia?

A
  • platelet count below 100,000 (bruise easily)
86
Q

What is hemophilia?

A
  • genetic lack of any clotting factor affects coagulation
  • sex-linked recessive in males (inherit from mother)
  • physical exertion causes bleeding and pain
87
Q

What is thrombosis?

A
  • abnormal clotting in unbroken vessel
  • most likely to occur in leg veins or inactive people
88
Q

What is a pulmonary embolism?

A
  • clot may break free, travel from veins to lungs
89
Q

What is an embolus?

A
  • anything that can travel in the blood and block blood vessels (clot, air bubbles)
90
Q

What is infarction?

A
  • tissue death
  • may occur if clot blocks blood supply to an organ (MI or stroke)
91
Q

What is Disseminated intravascular coagulation?

A

-Widespread clotting in unbroken vessels
- caused by septicemia (bacteria in blood) or cardiac arrest (heart stops beating causing the blood to stop moving, then clotting factors get activated)

92
Q

How can we prevent clots?

A
  • Vitamin K is required for formation of clotting factors
  • Vitamin K antagonists can be used to “thin” the blood and prevent clotting
  • Coumarin, warfarin, Vitamin K: blood thinners
  • Aspirin suppresses thromboxane A2
  • Dissolving clots that have already formed
  • Streptokinase: enzyme made by streptococci bacteria
  • Tissue plasminogen activator: works faster, is more specific, and now made by transgenic bacteria

Bio Exam 1: Blood (1 decks)

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