Circulatory System: Blood Flashcards

1
Q

Hematology

A

Branch of science that studies the blood, blood forming tissues and blood disorders

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2
Q

Functions of blood

A

Clotting - restricts fluid loss
Protection from disease and remove debris (use of macrophages)
- nutritive
-excretory function
-respiratory function
- transport of hormones and enzymes
- regulation of water and pH balance
- body temp
- protective functions (antibodies)

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3
Q

Blood matrix is called the _____

A

Plasma

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4
Q

Blood maintains a temperature of ____

A

38 degrees celsius

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5
Q

Blood pH

A

7.35-7.45

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6
Q

Adult Male blood volume

A

5-6L

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7
Q

Adult female blood volume

A

4-5L

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8
Q

Hematopoiesis

A

Production of the blood, especially the formed elements (RBCs, platelets, WBCS)

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9
Q

Where are formed elements produced

A

Red bone marrow

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10
Q

Where are lymphocytes produced?

A

Lymphoid tissue

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11
Q

Hemocytoblast

A

Originating hematopoietic stem cell

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12
Q

Erythropoiesis

A

Creation of RBCs

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13
Q

Flow of hematopoiesis

A
  1. Hemocytoblasts
  2. Myeloid stem cells
  3. Progenitor cells
  4. Blast cells
  5. Erythroblast stages
  6. Reticulocyte (still in bone marrow)
  7. Erythrocyte, a full mature formed element of blood
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14
Q

Function of erythrocytes

A
  1. Pick up O2 from lungs and deliver to tissues
  2. Pick of CO2 from tissue and unload it in lungs
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15
Q

Most abundant of all formed elements >99.9% is ____

A

Erythrocytes

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16
Q

Structure of erythrocytes

A
  • lack most organelles except the exoskeleton
  • biconcave disc shape allows for large SA = rapid exchange of O2, RBCs temporarily stack to make way through narrow vessels, strong flexible membrane allows them to deform without rupturing through small capillaries
  • no nucleus, ribosome, mitochondria = no repair
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17
Q

RBCs lifespan

A

About 120 days

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18
Q

Hematocrit

A

Percentage of blood volume occupied by RBCs

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19
Q

Normal Hct

A

Females 42%, males 46%

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20
Q

Anemia

A

Reduction in oxygen carrying capacity of the RBCs
Significant decrease in hematocrit is present
Different types: decrease in absolute number of RBCs or insufficient hemoglobin

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21
Q

Polycythemia

A

Increase in Hct is present (>65%)
Due to 1. Abnormal increase in RBC production or 2. Dehydration
Blood becomes viscous, hard for heart to pump, increased BP, increase risk for heart attack/stroke

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22
Q

Death of erythrocytes

A
  • macrophages in spleen, liver, red bone marrow phagocytize old RBCs
  • hemoglobin —> heme and globin
  • heme —> iron and biliverdin (green pigment)
  • iron binds with transferrin (transport protein) and some gets bound to ferritin (storage protein)
  • biliverdin —> bilirubin (yellow pigment)
  • bilirubin secreted into bile and converted to urobilinogen in feces
  • some urobilinogen reabsorbs into blood or converted to urobilin (yellow urine pigment)
  • most urobilinogen passes in feces as brown pigment called stercobilin
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23
Q

Erythrocytes production (erythropoiesis)

A

Occurs in red bone marrow
- takes 3-5 days
4 major steps:
1. Reduction in cell size
2. Increase in cell #
3. Synthesis of hemoglobin (erythroblast stage)
4. Loss of nucleus & other organelles (reticulocyte & mature RBC)
- production starts when HSC differentiates into erythrocyte CFU
—> in response to erythropoeitin becomes a proerythroblast —> erythroblast

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24
Q

Sickle cell disease

A

Abnormally shaped RBCs due to abnormality in gene
- RBCs clump and get stuck in small vessels
- cause pain and organ failure

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25
What determines ABO blood type?
The presence or absence of specific surface antigens attached to the RBC plasma membrane
26
What compose the surface antigens?
Glycolipidids (membrane phospholipids with short carbohydrate chains bonded to them)
27
Type a blood
RBCs only display antigen A Anti b antibody
28
Type B blood
Surface antigen B Anti-Bantibodies
29
Type AB blood
Surface antigens A and B Neither Anti-A nor anti-Bantibodies
30
Type O blood
Neither A nor B surface antigens Anti A and anti-Bantibodies
31
Agglutination occurs when ______
Plasma antibodies (agglutinins) bind to the antigens (agglutinogens) on the RBC plasma membrane and link the RBCs together forming an antibody-antigen complex
32
Universal donor
Type O-
33
Universal recipient
Type AB+
34
Rh blood type
Determined based on the presence or absence of the Rh antigen (aka D-antigen) - positive Rh displays Rh antigen - negative Rh does not display Rh antigen
35
Cross reaction
Transfusion of blood from someone with an incompatible blood group
36
Effects of a mismatched transfusion
- cross reaction - agglutination occurs and hemolysis of RBCs; several consequences: - disrupts oxygen carrying capacity - agglutinated cells block small blood vessels; damage to brain, heart, kidney - macrophages destroy agglutinated RBCs due to immune response releasing large amounts of hemoglobin; can lead to kidney failure due to recycling of Hb causing increase in bilirubin
37
Erythroblastosis fetalis
Second pregnancy with Rh+ fetus can result in HDN as the anti-Rh antibodies (mother is Rh-) cross placenta Prevention: injection of anti-Rh given before, during and after deliver, antibodies bind to and inactivate fetal Rh antigens so mothers immune doesn’t produce anti Rh-antibodies
38
Why collects from veins and not arteries?
1. Superficial veins - easier to locate 2. Vein walls = thinner and easier to penetrate than comparable sized arteries 3. Blood pressure lower in venous system, puncture seals quickly
39
5 types of WBCs
1. Neutrophils 2. Lymphocytes 3. Monocytes 4. Eosinophils 5. Basophils
40
5 types of WBCs
1. Neutrophils 2. Lymphocytes 3. Monocytes 4. Eosinophils 5. Basophils
41
Neutrophils
Most common WBC, present during acute infection
42
Lymphocytes
WBC seen during inflammation
43
Monocytes
WBCs that become macrophages after leaving blood stream - seen during chronic infection
44
Eosinophils
WBC during allergies and parasite infections
45
Basophils
- least common WBC - during allergic reaction - secrete histamine and heparin
46
WBC characteristics
- larger than RBCs - no hemoglobin - characterized based on presence or absence of granules when stained - most found in connective tissue and lymphatic system organs - only small # found in blood - emigration via diapedesis - ameboid movement - positive chemotaxis
47
Diapedesis
Process in which WBCs squeeze through endothelial cells
48
Ameboid movement
WBCs move like an amoeba
49
Leukopoeisis
WBCs develop from same hematopoietic stem cells in the red bone marrow as RBCs - colony forming unit cells give rise to three types of myeloblast cells, monoblast and lymphoblast cells
50
WBC seen during a blood smear
Mature WBCs are the cells you see when examining a blood smear when there is no pathology - presence of precursor cells is an indicator of pathology of the blood/bone marrow (e.g., lymphocytic leukemia)
51
Platelets originate from
Megakaryocytes (found in bone marrow)
52
Hormone that stimulates platelet production
Thrombopoietin (produced by kidneys)
53
Platelet life span
9-12 days, then removed by phagocytes in spleen
54
Platelets are important in _____ process
Clotting
55
Spleen is a ____ _____ ______
Platelet storage site; stores about 1/3 of all platelets, mobilize during circulatory crisis (severe bleeding)
56
3 major phases of hemostasis
A) vascular spasm B) platelet plug formation C) coagulation (clotting)
57
Vascular spasm
Smooth muscle in vessel wall contracts, this decreases blood flow and limits blood loss; endothelial cells (lining blood vessel wall) become sticky which allows platelets to adhere
58
Platelet plug formation
Platelets release chemicals to initiate and control clotting and form a temporary patch in walls of damaged blood vessels - i) platelet adhesion: platelets stick to damaged blood vessel and release chemicals to attract more platelets - ii) positive feedback loop with more platelets adhering to produce “platelet plug”
59
Coagulation (clotting)
The clotting cascade is a complex of series of chemical reactions that result in a clot that consists of a network of insoluble protein fibres called fibrin
60
Point of hemostasis
A sequence of responses that stop bleeding
61
3 main coagulation pathways
1. Extrinsic pathway/mechanism 2. Intrinsic/pathway mechanism 3. Common pathway
62
Extrinsic pathway/mechanism
Initiated by damaged blood vessel walls that release tissue factor (Factor III) Tissue factor starts a series of reactions to activate Factor X
63
Intrinsic/pathway mechanism
Initiated in the bloodstream by the activation of factor XII Factor XII begins a sequence of reactions that also activate factor X
64
Common pathway
Factor X activates a sequence of reactions that lead to conversion of the soluble plasma protein fibrinogen into soluble threads of the protein fibrin
65
Blood clotting also requires:
Vitamin K and calcium to synthesize some clotting factors
66
Vitamin K deficiency
Causes malabsorption of lipids, use of antibiotics that kill the “good” bacteria in the large intestine
67
Leukemia
Many lymphoblasts will be seen in a blood smear
68
Hemophilia
Blood disorder caused by lack of or inaction of one or more clotting factor
69
Thrombosis
Clotting that occurs in an unbroken blood vessel Caused by roughened blood vessel surfaces from artherosclerosis, trauma or infection causing platelets to adhere and form a thrombus
70
Most common hemophilia
Type A, missing VIII clotting factor
71
Hemophilia A symptoms
Severe hemorrhage after minor injuries, frequent nose bleeds, hemtomas, blood in urine
72
Embolus
A thrombus, air bubble, fat from broken bones, debris transported by the bloodstream that moves from its site of origin
73
Anticoagulant
A substance that delays or prevents blood clotting
74
Heparin
Anticoagulant given during open heart surgery to maintain blood flow
75
Warfarin
Anticoagulant Prevents strokes and heart attacks, especially after a blood clot