BLOOD Flashcards
(88 cards)
1
Q
Alkilosis
A
Blood pH above 7.45
2
Q
Acidosis
A
Blood pH below 7.35
3
Q
% body weight composition of blood
A
8%
4
Q
Plasma
A
Non-living fluid matrix
5
Q
Formed elements
A
Living Blood “Cells”
6
Q
Erythrocytes
A
Red Blood Cells
7
Q
Leukocytes
A
White Blood Cells
8
Q
Dissolved solutes in blood
A
Nutrients, gases, hormones, wastes, proteins, and inorganic ions
8
Q
Platelets
A
Thrombocytes, cell fragments
9
Q
Plasma proteins most abundant solutes
A
Albumin, globulin, fibrinogen
10
Q
Albumin
A
Osmotic balance and buffers pH
11
Q
Globulins
A
Immune response & lipid transport
11
Q
Fibrinogen
A
Blood Clotting
12
Q
Leukocytes make up _____% of total blood volume
A
<1% (Close to 0.1%)
13
Q
Leukocytosis
A
WBC Count > 11,000/uL
14
Q
Diapedesis
A
Process of WBC’s passing through capillary walls into surrounding tissue
15
Q
Granulocytes
A
Visible cytoplasmic granules (Neutrophils, eosinophils, basophils)
16
Q
Agranulocytes
A
No visible cytoplasmic granules (Lymphocytes & Monocytes)
17
Q
Buffy coat
A
Leukocytes & Platelets
18
Q
Neutrophils
A
-Polymorphonuclear leukocytes
-Very phagocytic
19
Q
Eosinophils
A
-Lysozyme-like granules
-Allergies, asthma, and general immune response
20
Q
Lymphocytes
A
-Mainly in lymphocyte tissue
-T Lymphocytes (Against virus-infected cell & tumor cells)
B Lymphocytes (Antibody producing cells)
21
Q
Monocytes
A
-Leave circulation to enter tissue
-Actively phagocytic cells
-Activates lymphocytes
21
Q
Spectrin
A
Plasma membrane protein of erythrocytes
22
Basophils
Granules contain histamine (inflammatory chemical)
23
Platelets
-Cytoplasmic fragments of megakaryocytes
-Act in clotting process
23
Myeloid Stem cell fate
All other cell types
24
Lymphoid stem cell fate
B & T Lymphocytes
25
Thrombopoietin
Regulator for formation of platelets
26
Lifespan of erythrocyres
100-120 days
27
Hematopoietic Stem Cells
Stem cells giving rise to blood cells
28
Carbamino hemoglobin
CO2 binding to hemoglobin
28
Percent hemoglobin composition in erythrocytes
97%
29
Hematopoietic stem ells
Stem cells that give rise to all formed elements of blood
30
Hematocrit
Packed cell volume
31
Hematocrit levels in men & women
-47% ± 5 for males
-42% ± 5 for females
32
Formula for hematocrit
Volume of RBC/Volume of total blood
33
Causes/Signs of high hematocrit
-Dehydration
-Polycythemia Vera: Disease of bone marrow forming too many RBC's
-Lung/Heart Disease: Low oxygen triggering too much RBC production
34
Cause of blue horse shoe crab blood
Copper acting as heme instead of iron
35
Too much erythrpoiesis
Increased blood viscosity
36
Too little erythropoiesis
Tissue Hypoxia
37
Erythropoietin
Hormone released by kidneys that directly stimulates erythropoiesis
38
Affect of testosterone
Increased erythropoiesis causing high RBC count in males
39
Bodies response to hypoxia
Kidneys release erythropoietin causing growth of red bone marrow and an increase in RBC count which allows blood to carry more O2
40
Impact of kidney failure & dialysis on blood
No production of EPO from kidneys causing an increase count in RBCs
41
Causes of hypoxia
-Decreased RBC number
-Insufficient hemoglobin per RBC
-Reduced availability of O2
42
Reasons for having an increased risk of stroke while at high altitude
Low environmental oxygen levels causing tissue hypoxia which leads to overproduction of RBC's causing increase in blood viscosity
43
Effects of EPO
-Rapid maturation of committed marrow cells
-Increased circulating reticulocyte count in 1-2 days
44
Fate of erythrocytes as they age
Degredation due to a loss of spectrin and end up in the spleen to be englufed by macrophages
45
Fate of heme during RBC destrction
Degraded into liver bilirubin. Liver will secrete this bilirubin to serve the production of bile which aids in lipid digestion. Bilirubin will event degrade into a pigment that we excrete in feces. Iron is salvaged for reuse.
46
Fate of globin in RBC destruction
Metabolized into amino acids that are released for recirculation and re-uptaken by cells for protein synthesis
47
Cause of renal anemia
Lack of EPO often due to renal disease
48
Cause of aplastic anemia
Destruction or inhibition of red marrow. Often treated with transfusions or transplanted stem cells.
49
Cause of hemolytic anemias
Premature RBC lysis causes by hemoglobin abnormalities, incompatible transfusions, or infections
50
Thalassemia
-Typically meditteranean ancestry
-One faulty or missing globin chain causing thin and delicate RBCs.
51
Sickle Cell anemia
-One amino acid wrong in globin beta chain of hemoglobin causing crescent shaped RBCs when blood has low O2.
-RBC's can rupture easily and can block capillaries and small vessels
52
Malaria in sickle cell anemia
Parasite is unable to mature giving immune properties to host
53
Polycethemia Vera
"True" increased RBC Count
-Bone marrow cancer can create excess RBC's causing an increase in blood viscosity
54
Secondary polycythemia
-Less O2 available causing an increase production in EPO leading to increased RBC count
-Leads to a lower plasma volume
-Used in blood doping
55
Hemostasis
-Series of reactions for stoppage of bleeding
-Requires clotting factors & substances released by platelets and injured tissues
56
Three steps of hemostasis
1. Vascular spasm
2. Platelet plug formation
3. Coagulation
57
Vasoconstriction
Paracrine molecule signaling for the constriction of blood vessels. Secretion of these signals is promoted by the breaking of vessels & endothelial cells
58
Plug formation
Activated platelets form a temporary platelet plug that is made by sticking of platelets to collagen fibers by von Willebrand factor.
59
Signals that promote platelet accumulation
-ADP
-Serotonin and thromboxane A2
-Ca2+
60
Impact of platelet interaction with collagen
Activation of platelet synthesis
61
Properties of coagulation
Must remain local as surrounding cells must prevent accumulation of clotting
62
Intrinsic coagulation
Triggered by factors within the blood/blood vessel
63
Extrinsic coagulation
Triggered by factors outside the blood/blood vessel
64
Contact activation or intrinsic pathway
Triggered by negatively charged surfaces
-Activated platelets
-Collagen
65
Tissue factors or extrinisc pathway
Triggered by exposure to tissue factor or factor III-Significantly faster due to less reactions being needed
66
Three phases of coagulation
1. Prothrombin activator formation
2. Prothrombin converted to enzyme thrombin
3. Thrombin catalyzes fibrinogen--> fibrin
67
Role of platelet-derived growth factor
Division of smooth muscle cells and fibroblasts to rebuild blood vessel outer walls
68
Role of vascular endothelial growth factor
Restores endothelial lining
69
Fibrinolysis
-Removes unneeded clots after healing
-Begins within 2 days and continues for several days
70
Plasmin
Fibrin digesting enzyme
-Produced by activated plasminogen
-Trapped during clot formation causing a negative feedback loop
71
Thrombus
Blood clot
72
Embolus
Unattached mass that travels in the bloodstream
73
Thrombocytopenia
Deficient number of circulating platelets
-Platelet count <50,000/uL
-Treated with transfusion of concentrated platelets
-Petechiae appear due to spontaneous wide spread hemorrhage
74
Reasons for an inability to synthesize procoagulants
-Impaired liver function
-Caused by vitamin K deficiency, hepatitis, and cirrhosis
75
Hemophilia A
Factor VIII deficiency (77% of all cases)
76
Hemophilia B
Factor IX deficiency
77
Hemophilia C
Mild type; factor XI deficiency
78
Disseminated intravascular coagulation
Widespread clotting of an intact vessel combined with severe bleeding
79
Causes of disseminated intravascular coagulation
Usually pregnancy complications or incompatible blood transfusions that result in adverse reactions
80
Reason for aspirin to not be instructed before surgery
Acetylsalicylic acid acts as an anti-thrombotic drug preventing the activation of thromboxane and prostaglandin. Therefore, no possible plug formation to stop bleeding in intrinsic pathways
81
Life Span of Platelets
10 days
82
Area of blood cell formation in bone marrow
Axial skeleton, girdles, and proximal epiphysis of humerus and femur.
83
Reason to give children vitamin K shots
In order to have the means necessary to form clots an infant may not otherwise be able to heal
