blood Flashcards
1
Q
components of whole blood (3)
A
plasma
platlets
leukocytes (5)
plasma (matrix) plus formed elements
2
Q
2 categories/ 5 kinds of Leukocytes
A
granulocytes: neutrophils, eosinophils, basophils
agranulocytes: lymphocytes, monocytes
3
Q
circulatory vs. cardiovascular system
A
circ: heart, blood vessels, AND blood
cardio: only heart, blood vessels
4
Q
3 functions of the circulatory system
A
transport
protection
regulation
5
Q
How transport?
A
O2, CO2
nutrients
waste to kidneys
hormones to organs
stem cells bone to tissues
6
Q
How protect?
A
inflammation helps guard against infection
destroy harmful organisms/cancer cells
clotting
7
Q
How regulates?
A
fluid balance (osmolarity regulation)
pH of extracellular fluids
regulating body temperature (pee more in winter)
8
Q
hematocrit layers (3)
A
bottom is the erythrocytes
buffy coat WBCs and platelets <1%
plasma
9
Q
serum vs. plasma
A
same as plasma with clots removed (no fibrinogen)
10
Q
plasma
A
liquid of blood
11
Q
3 plasma proteins
A
albumin - smallest, viscosity/osmolarity, most of globulins - (antibodies) alpha, beta, gamma fibrinogen - pre-clotting fiber
12
Q
plasma proteins formed?
A
liver - albumin and globulins plasma cells- fibrinogen
13
Q
plasma components
A
water, proteins, nutrients (glucose, vitamins, fats, minerals), electrolytes (Na+/Sodium), nitrogenous wastes (urea, toxic catabolic products), hormones, gasses (O2,CO2, Nitrogen)
14
Q
viscosity? water vs. whole blood vs. plasma?
A
viscosity - how thin/thick “sticky” whole blood x4.5-5.5 as water plasma x2 as water
15
Q
blood pressure if osmolarity is too high
A
too much water in blood = high BP
16
Q
blood pressure if osmolarity is too low
A
too much water in tissues = low BP/ edema
17
Q
osmolarity
A
molarity of dissolved particles that cannot pass through blood vessel wall electrolyte (sodium)/protein/RBC-water balance
18
Q
hypoproteinemia
A
too little plasma proteins starvation, liver/kidney diseases, severe burns
19
Q
kwashiorker
A
severe protein deficiency thin arms/swollen belly/fed cereals (after weaned)
20
Q
hemopoiesis
A
making blood/ formed elements
21
Q
colloid osmotic pressure (COP)
A
protein relationship to blood osmotic pressure *ed up in kwashiorker - edema, big belly, diarrhea, dehydration
22
Q
hemopoetic tissues
A
tissues that make blood cells: embryo-yolk sac infancy on- red bone marrow makes 7 formed elements lymphocytes- made in lymphatic tissues (thymus, tonsils, lymph nodes, spleen, mucous membranes)
23
Q
plasma replacement
A
water - mostly from digestive tract electrolytes/nutrients-dig. Tract gamma globulins- conn. Tissue plasma cells proteins-liver
24
Q
RBC characteristics
A
biconcave no nucleus/mitochondria anaerobic fermentation to make ATP plasma mem. Glycolipids - determine blood type cytoplasm-carbonic anahydrase (CAH)- role in gas transport/pH balance
25
% of RBC cytoplasm that is hemoglobin
33%
26
RBC functions
O2 from lungs to tissues CO2 from tissues to lungs
27
Hemoglobin structure
4 protein chains - globins adult - 2 alpha, 2 beta chains fetal- 2 alpha, 2 gamma 4 heme groups (bind O2 to ferrous ion Fe at center)
28
2 factors determine O2 in blood
RBC and hemoglobin concentration
29
RBC: hematocrit vs. hemoglobin concentration
hematocrit - %of RBC in total blood volume - 42-52% M, 37048%W; hemoglobin conc. - how much hemoglobin in blood (determines delivery of O2 and CO2) - usually 13-18 in men 12-16 in women
30
erythropoiesis: hemopoietic stem cell, colony-forming unit, erythroblast, reticulocyte, erythrocyte
making of RBC - 3-5 days
31
correction of hypoxemia
O2 defficiency in blood, ex. Hemmorhaging negative feedback loop kidneys detect and increase erythropoietin excretion stimulates red bone marrow accelerated erythropoiesis increased RBC count increased O2 transport
32
emphysema (hypoxemia)
less lung tissue is available to oxygenate blood kidneys/marrow increase RBC count and cause polycythemia
33
AKA "erythrocyte graveyard"
spleen, enlarged may mean disease with too many RBC breaking down
34
sickle cell anemia process
hereditary hemoglobin defect mostly Africa and Mediterranean descent recessive alle modifies hemoglobin HbS instead of HbA HbS doesn't bind O2 well so becomes long and pointy sticky, clumpy (agglutinate) block small vessels, cause intense pain in O2 starved tissues hemolysis of cells (cell rupture) causes anemia results in hypoxemia triggers further sickling deadly positive feedback loop spleen becomes enlarged and fibrous
35
2 kinds of sickle cell carriers
homozygous - exhibit disease heterozygous - have trait but rarely symptoms, makes resistant to malaria; 2 heterozygous parents have 25% of homozygous child
36
hemolysis
rupture of RBCs, releasing hemoglobin and leaving membrane
37
aged/damaged RBC recycling
membrane frags - digested by macrophages in liver/spleen hemoglobin- macrophages separate heme from globin globin-free amino acids heme- iron removed andrecycled into the blood rest-biliverdin (greenish pigment)- bilirubin - binds to albumin in blood plasma liver removes from albumin-secretes in bilein gallbladder- small intestines - bacteria turns to urobilinogen (brown feces) and urochrome (yellow urine)
38
jaundice
sign of rapid hemolysis, liver disease, or bile duct obstruction
39
can be caused by hemoglobin blocking kidney tubules
renal failure
40
antigens
molecules on surface of cell membrane activate an immune response genetically unique to individual foreign antigen causes immune response
41
agglutinogens
antigens on surface of RBCs that are basis of blood typing
42
blood typing ABO: antigens and antibodies
ABO group - A,B,AB, O A carries A antigens and is Anti-B, B carries B antigens Anti-A, AB has both A and B antigens and carries no antibodies, O has neither antigen carries Anti-A and Anti-B
43
Most common, rarest ABO blood types
O is most common AB is most rare
44
ABO and Rh incompatabilities
RH+ if have the D antigen (DD or Dd) - is not normally present; and Rh- if don't have the D antigen (dd); If RH- is exposed to RH+ then forms antibodies; RhoGAM shot binds fetal agglutinogens in her blood so she won't form anti-D antibodies
45
erythroblastic fetalis or hemolytic disease of the newborn (HDN)
cross-reaction fetus/maternal blood types baby is born with hemolytic anemia HDN if Mom passes anti-D antibodies through placenta and agglutinates fetal erythrocytes
46
prevention of fetus/maturnal reactions
RhoGAM given to pregnant Rh- Mom with Rh+ child so won't form anti-D antibodies
47
all leukocyte characteristics
protect against infection/disease conspicuous nuclei spend only a few hours in bloodstream retain organelles
48
structure, function, %: neutrophils
granulocyte; most abundant WBC 60-70% nucleus with 3-5 lobes aggressively antibacterial
49
structure, function, %: eosinophils
granulocyte; only 2-4% of WBCs bilobed (sand timer) phagocytize inflammatory chemicals, allergens, destroy large parasitic worms
50
structure, function, %: basophils
granulocyte; rarest WBC
51
of chem. Reaction in coagulation
over 30
52
#s of clotting reactions
order of discovery NOT order of occurance
53
protein gamma globulin AKA
antibodies
54
plasma
liquid of blood
55
3 plasma proteins
albumin - smallest, viscosity/osmolarity, most of globulins - (antibodies) alpha, beta, gamma fibrinogen - pre-clotting fiber
56
plasma proteins formed?
liver - albumin and globulins plasma cells- fibrinogen
57
plasma components
water, proteins, nutrients (glucose, vitamins, fats, minerals), electrolytes (Na+/Sodium), nitrogenous wastes (urea, toxic catabolic products), hormones, gasses (O2,CO2, Nitrogen)
58
viscosity? water vs. whole blood vs. plasma?
viscosity - how thin/thick "sticky" whole blood x4.5-5.5 as water plasma x2 as water
59
blood pressure if osmolarity is too high
too much water in blood = high BP
60
blood pressure if osmolarity is too low
too much water in tissues = low BP/ edema
61
osmolarity
molarity of dissolved particles that cannot pass through blood vessel wall electrolyte (sodium)/protein/RBC-water balance
62
hypoproteinemia
too little plasma proteins starvation, liver/kidney diseases, severe burns
63
kwashiorker
severe protein deficiency thin arms/swollen belly/fed cereals (after weaned)
64
hemopoiesis
making blood/ formed elements
65
colloid osmotic pressure (COP)
protein relationship to blood osmotic pressure \*ed up in kwashiorker - edema, big belly, diarrhea, dehydration
66
hemopoetic tissues
tissues that make blood cells: embryo-yolk sac infancy on- red bone marrow makes 7 formed elements lymphocytes- made in lymphatic tissues (thymus, tonsils, lymph nodes, spleen, mucous membranes)
67
plasma replacement
water - mostly from digestive tract electrolytes/nutrients-dig. Tract gamma globulins- conn. Tissue plasma cells proteins-liver
68
RBC characteristics
biconcave no nucleus/mitochondria anaerobic fermentation to make ATP plasma mem. Glycolipids - determine blood type cytoplasm-carbonic anahydrase (CAH)- role in gas transport/pH balance
69
% of RBC cytoplasm that is hemoglobin
33 percent
70
RBC functions
O2 from lungs to tissues CO2 from tissues to lungs
71
Hemoglobin structure
4 protein chains - globins adult - 2 alpha, 2 beta chains fetal- 2 alpha, 2 gamma 4 heme groups (bind O2 to ferrous ion Fe at center)
72
2 factors determine O2 in blood
RBC and hemoglobin concentration
73
RBC: hematocrit vs. hemoglobin concentration
hematocrit - %of RBC in total blood volume - 42-52% M, 37048%W; hemoglobin conc. - how much hemoglobin in blood (determines delivery of O2 and CO2) - usually 13-18 in men 12-16 in women
74
erythropoiesis: hemopoietic stem cell, colony-forming unit, erythroblast, reticulocyte, erythrocyte
making of RBC - 3-5 days
75
correction of hypoxemia
O2 defficiency in blood, ex. Hemmorhaging negative feedback loop kidneys detect and increase erythropoietin excretion stimulates red bone marrow accelerated erythropoiesis increased RBC count increased O2 transport
76
emphysema (hypoxemia)
less lung tissue is available to oxygenate blood kidneys/marrow increase RBC count and cause polycythemia
77
AKA "erythrocyte graveyard"
spleen, enlarged may mean disease with too many RBC breaking down
78
sickle cell anemia process
hereditary hemoglobin defect mostly Africa and Mediterranean descent recessive alle modifies hemoglobin HbS instead of HbA HbS doesn't bind O2 well so becomes long and pointy sticky, clumpy (agglutinate) block small vessels, cause intense pain in O2 starved tissues hemolysis of cells (cell rupture) causes anemia results in hypoxemia triggers further sickling deadly positive feedback loop spleen becomes enlarged and fibrous
79
2 kinds of sickle cell carriers
homozygous - exhibit disease heterozygous - have trait but rarely symptoms, makes resistant to malaria; 2 heterozygous parents have 25% of homozygous child
80
hemolysis
rupture of RBCs, releasing hemoglobin and leaving membrane
81
aged/damaged RBC recycling
membrane frags - digested by macrophages in liver/spleen hemoglobin- macrophages separate heme from globin globin-free amino acids heme- iron removed andrecycled into the blood rest-biliverdin (greenish pigment)- bilirubin - binds to albumin in blood plasma liver removes from albumin-secretes in bilein gallbladder- small intestines - bacteria turns to urobilinogen (brown feces) and urochrome (yellow urine)
82
jaundice
sign of rapid hemolysis, liver disease, or bile duct obstruction
83
can be caused by hemoglobin blocking kidney tubules
renal failure
84
antigens
molecules on surface of cell membrane activate an immune response genetically unique to individual foreign antigen causes immune response
85
agglutinogens
antigens on surface of RBCs that are basis of blood typing
86
blood typing ABO: antigens and antibodies
ABO group - A,B,AB, O A carries A antigens and is Anti-B, B carries B antigens Anti-A, AB has both A and B antigens and carries no antibodies, O has neither antigen carries Anti-A and Anti-B
87
Most common, rarest ABO blood types
O is most common AB is most rare
88
ABO and Rh incompatabilities
RH+ if have the D antigen (DD or Dd) - is not normally present; and Rh- if don't have the D antigen (dd); If RH- is exposed to RH+ then forms antibodies; RhoGAM shot binds fetal agglutinogens in her blood so she won't form anti-D antibodies
89
erythroblastic fetalis or hemolytic disease of the newborn (HDN)
cross-reaction fetus/maternal blood types baby is born with hemolytic anemia HDN if Mom passes anti-D antibodies through placenta and agglutinates fetal erythrocytes
90
prevention of fetus/maturnal reactions
RhoGAM given to pregnant Rh- Mom with Rh+ child so won't form anti-D antibodies
91
all leukocyte characteristics
protect against infection/disease conspicuous nuclei spend only a few hours in bloodstream retain organelles
92
structure, function, %: neutrophils
granulocyte; most abundant WBC 60-70% nucleus with 3-5 lobes aggressively antibacterial
93
structure, function, %: eosinophils
granulocyte; only 2-4% of WBCs bilobed (sand timer) phagocytize inflammatory chemicals, allergens, destroy large parasitic worms
94
structure, function, %: basophils
granulocyte; rarest WBC
95
of chem. Reaction in coagulation
over 30
96
#s of clotting reactions
order of discovery NOT order of occurance
97
protein gamma globulin AKA
antibodies
98
plasma
liquid of blood
99
3 plasma proteins
albumin - smallest, viscosity/osmolarity, most of globulins - (antibodies) alpha, beta, gamma fibrinogen - pre-clotting fiber
100
plasma proteins formed?
liver - albumin and globulins plasma cells- fibrinogen
101
plasma components
water, proteins, nutrients (glucose, vitamins, fats, minerals), electrolytes (Na+/Sodium), nitrogenous wastes (urea, toxic catabolic products), hormones, gasses (O2,CO2, Nitrogen)
102
viscosity? water vs. whole blood vs. plasma?
viscosity - how thin/thick "sticky" whole blood x4.5-5.5 as water plasma x2 as water
103
blood pressure if osmolarity is too high
too much water in blood = high BP
104
blood pressure if osmolarity is too low
too much water in tissues = low BP/ edema
105
osmolarity
molarity of dissolved particles that cannot pass through blood vessel wall electrolyte (sodium)/protein/RBC-water balance
106
hypoproteinemia
too little plasma proteins starvation, liver/kidney diseases, severe burns
107
kwashiorker
severe protein deficiency thin arms/swollen belly/fed cereals (after weaned)
108
hemopoiesis
making blood/ formed elements
109
colloid osmotic pressure (COP)
protein relationship to blood osmotic pressure \*ed up in kwashiorker - edema, big belly, diarrhea, dehydration
110
hemopoetic tissues
tissues that make blood cells: embryo-yolk sac infancy on- red bone marrow makes 7 formed elements lymphocytes- made in lymphatic tissues (thymus, tonsils, lymph nodes, spleen, mucous membranes)
111
plasma replacement
water - mostly from digestive tract electrolytes/nutrients-dig. Tract gamma globulins- conn. Tissue plasma cells proteins-liver
112
RBC characteristics
biconcave no nucleus/mitochondria anaerobic fermentation to make ATP plasma mem. Glycolipids - determine blood type cytoplasm-carbonic anahydrase (CAH)- role in gas transport/pH balance
113
% of RBC cytoplasm that is hemoglobin
33 percent
114
RBC functions
O2 from lungs to tissues CO2 from tissues to lungs
115
Hemoglobin structure
4 protein chains - globins adult - 2 alpha, 2 beta chains fetal- 2 alpha, 2 gamma 4 heme groups (bind O2 to ferrous ion Fe at center)
116
2 factors determine O2 in blood
RBC and hemoglobin concentration
117
RBC: hematocrit vs. hemoglobin concentration
hematocrit - %of RBC in total blood volume - 42-52% M, 37048%W; hemoglobin conc. - how much hemoglobin in blood (determines delivery of O2 and CO2) - usually 13-18 in men 12-16 in women
118
erythropoiesis: hemopoietic stem cell, colony-forming unit, erythroblast, reticulocyte, erythrocyte
making of RBC - 3-5 days
119
correction of hypoxemia
O2 defficiency in blood, ex. Hemmorhaging negative feedback loop kidneys detect and increase erythropoietin excretion stimulates red bone marrow accelerated erythropoiesis increased RBC count increased O2 transport
120
emphysema (hypoxemia)
less lung tissue is available to oxygenate blood kidneys/marrow increase RBC count and cause polycythemia
121
AKA "erythrocyte graveyard"
spleen, enlarged may mean disease with too many RBC breaking down
122
sickle cell anemia process
hereditary hemoglobin defect mostly Africa and Mediterranean descent recessive alle modifies hemoglobin HbS instead of HbA HbS doesn't bind O2 well so becomes long and pointy sticky, clumpy (agglutinate) block small vessels, cause intense pain in O2 starved tissues hemolysis of cells (cell rupture) causes anemia results in hypoxemia triggers further sickling deadly positive feedback loop spleen becomes enlarged and fibrous
123
2 kinds of sickle cell carriers
homozygous - exhibit disease heterozygous - have trait but rarely symptoms, makes resistant to malaria; 2 heterozygous parents have 25% of homozygous child
124
hemolysis
rupture of RBCs, releasing hemoglobin and leaving membrane
125
aged/damaged RBC recycling
membrane frags - digested by macrophages in liver/spleen hemoglobin- macrophages separate heme from globin globin-free amino acids heme- iron removed andrecycled into the blood rest-biliverdin (greenish pigment)- bilirubin - binds to albumin in blood plasma liver removes from albumin-secretes in bilein gallbladder- small intestines - bacteria turns to urobilinogen (brown feces) and urochrome (yellow urine)
126
jaundice
sign of rapid hemolysis, liver disease, or bile duct obstruction
127
can be caused by hemoglobin blocking kidney tubules
renal failure
128
antigens
molecules on surface of cell membrane activate an immune response genetically unique to individual foreign antigen causes immune response
129
agglutinogens
antigens on surface of RBCs that are basis of blood typing
130
blood typing ABO: antigens and antibodies
ABO group - A,B,AB, O A carries A antigens and is Anti-B, B carries B antigens Anti-A, AB has both A and B antigens and carries no antibodies, O has neither antigen carries Anti-A and Anti-B
131
Most common, rarest ABO blood types
O is most common AB is most rare
132
ABO and Rh incompatabilities
RH+ if have the D antigen (DD or Dd) - is not normally present; and Rh- if don't have the D antigen (dd); If RH- is exposed to RH+ then forms antibodies; RhoGAM shot binds fetal agglutinogens in her blood so she won't form anti-D antibodies
133
erythroblastic fetalis or hemolytic disease of the newborn (HDN)
cross-reaction fetus/maternal blood types baby is born with hemolytic anemia HDN if Mom passes anti-D antibodies through placenta and agglutinates fetal erythrocytes
134
prevention of fetus/maturnal reactions
RhoGAM given to pregnant Rh- Mom with Rh+ child so won't form anti-D antibodies
135
all leukocyte characteristics
protect against infection/disease conspicuous nuclei spend only a few hours in bloodstream retain organelles
136
structure, function, %: neutrophils
granulocyte; most abundant WBC 60-70% nucleus with 3-5 lobes aggressively antibacterial
137
structure, function, %: eosinophils
granulocyte; only 2-4% of WBCs bilobed (sand timer) phagocytize inflammatory chemicals, allergens, destroy large parasitic worms
138
structure, function, %: basophils
granulocyte; rarest WBC
139
of chem. Reaction in coagulation
over 30
140
#s of clotting reactions
order of discovery NOT order of occurance
141
protein gamma globulin AKA
antibodies
