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BSCI202: Anatomy & Physiology II > BLOOD > Flashcards

BLOOD Flashcards

1
Q

Alkilosis

A

Blood pH above 7.45

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2
Q

Acidosis

A

Blood pH below 7.35

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3
Q

% body weight composition of blood

A

8%

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4
Q

Plasma

A

Non-living fluid matrix

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5
Q

Formed elements

A

Living Blood “Cells”

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6
Q

Erythrocytes

A

Red Blood Cells

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7
Q

Leukocytes

A

White Blood Cells

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8
Q

Dissolved solutes in blood

A

Nutrients, gases, hormones, wastes, proteins, and inorganic ions

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8
Q

Platelets

A

Thrombocytes, cell fragments

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9
Q

Plasma proteins most abundant solutes

A

Albumin, globulin, fibrinogen

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10
Q

Albumin

A

Osmotic balance and buffers pH

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11
Q

Globulins

A

Immune response & lipid transport

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11
Q

Fibrinogen

A

Blood Clotting

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12
Q

Leukocytes make up _____% of total blood volume

A

<1% (Close to 0.1%)

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13
Q

Leukocytosis

A

WBC Count > 11,000/uL

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14
Q

Diapedesis

A

Process of WBC’s passing through capillary walls into surrounding tissue

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15
Q

Granulocytes

A

Visible cytoplasmic granules (Neutrophils, eosinophils, basophils)

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16
Q

Agranulocytes

A

No visible cytoplasmic granules (Lymphocytes & Monocytes)

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17
Q

Buffy coat

A

Leukocytes & Platelets

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18
Q

Neutrophils

A

-Polymorphonuclear leukocytes
-Very phagocytic

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19
Q

Eosinophils

A

-Lysozyme-like granules
-Allergies, asthma, and general immune response

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20
Q

Lymphocytes

A

-Mainly in lymphocyte tissue
-T Lymphocytes (Against virus-infected cell & tumor cells)
B Lymphocytes (Antibody producing cells)

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21
Q

Monocytes

A

-Leave circulation to enter tissue
-Actively phagocytic cells
-Activates lymphocytes

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21
Q

Spectrin

A

Plasma membrane protein of erythrocytes

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22
Q

Basophils

A

Granules contain histamine (inflammatory chemical)

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23
Q

Platelets

A

-Cytoplasmic fragments of megakaryocytes
-Act in clotting process

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23
Q

Myeloid Stem cell fate

A

All other cell types

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24
Q

Lymphoid stem cell fate

A

B & T Lymphocytes

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25
Q

Thrombopoietin

A

Regulator for formation of platelets

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26
Q

Lifespan of erythrocyres

A

100-120 days

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27
Q

Hematopoietic Stem Cells

A

Stem cells giving rise to blood cells

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28
Q

Carbamino hemoglobin

A

CO2 binding to hemoglobin

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28
Q

Percent hemoglobin composition in erythrocytes

A

97%

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29
Q

Hematopoietic stem ells

A

Stem cells that give rise to all formed elements of blood

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30
Q

Hematocrit

A

Packed cell volume

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31
Q

Hematocrit levels in men & women

A

-47% ± 5 for males
-42% ± 5 for females

32
Q

Formula for hematocrit

A

Volume of RBC/Volume of total blood

33
Q

Causes/Signs of high hematocrit

A

-Dehydration
-Polycythemia Vera: Disease of bone marrow forming too many RBC’s
-Lung/Heart Disease: Low oxygen triggering too much RBC production

34
Q

Cause of blue horse shoe crab blood

A

Copper acting as heme instead of iron

35
Q

Too much erythrpoiesis

A

Increased blood viscosity

36
Q

Too little erythropoiesis

A

Tissue Hypoxia

37
Q

Erythropoietin

A

Hormone released by kidneys that directly stimulates erythropoiesis

38
Q

Affect of testosterone

A

Increased erythropoiesis causing high RBC count in males

39
Q

Bodies response to hypoxia

A

Kidneys release erythropoietin causing growth of red bone marrow and an increase in RBC count which allows blood to carry more O2

40
Q

Impact of kidney failure & dialysis on blood

A

No production of EPO from kidneys causing an increase count in RBCs

41
Q

Causes of hypoxia

A

-Decreased RBC number
-Insufficient hemoglobin per RBC
-Reduced availability of O2

42
Q

Reasons for having an increased risk of stroke while at high altitude

A

Low environmental oxygen levels causing tissue hypoxia which leads to overproduction of RBC’s causing increase in blood viscosity

43
Q

Effects of EPO

A

-Rapid maturation of committed marrow cells
-Increased circulating reticulocyte count in 1-2 days

44
Q

Fate of erythrocytes as they age

A

Degredation due to a loss of spectrin and end up in the spleen to be englufed by macrophages

45
Q

Fate of heme during RBC destrction

A

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
Q

Fate of globin in RBC destruction

A

Metabolized into amino acids that are released for recirculation and re-uptaken by cells for protein synthesis

47
Q

Cause of renal anemia

A

Lack of EPO often due to renal disease

48
Q

Cause of aplastic anemia

A

Destruction or inhibition of red marrow. Often treated with transfusions or transplanted stem cells.

49
Q

Cause of hemolytic anemias

A

Premature RBC lysis causes by hemoglobin abnormalities, incompatible transfusions, or infections

50
Q

Thalassemia

A

-Typically meditteranean ancestry
-One faulty or missing globin chain causing thin and delicate RBCs.

51
Q

Sickle Cell anemia

A

-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
Q

Malaria in sickle cell anemia

A

Parasite is unable to mature giving immune properties to host

53
Q

Polycethemia Vera

A

“True” increased RBC Count
-Bone marrow cancer can create excess RBC’s causing an increase in blood viscosity

54
Q

Secondary polycythemia

A

-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
Q

Hemostasis

A

-Series of reactions for stoppage of bleeding
-Requires clotting factors & substances released by platelets and injured tissues

56
Q

Three steps of hemostasis

A
  1. Vascular spasm
  2. Platelet plug formation
  3. Coagulation
57
Q

Vasoconstriction

A

Paracrine molecule signaling for the constriction of blood vessels. Secretion of these signals is promoted by the breaking of vessels & endothelial cells

58
Q

Plug formation

A

Activated platelets form a temporary platelet plug that is made by sticking of platelets to collagen fibers by von Willebrand factor.

59
Q

Signals that promote platelet accumulation

A

-ADP
-Serotonin and thromboxane A2
-Ca2+

60
Q

Impact of platelet interaction with collagen

A

Activation of platelet synthesis

61
Q

Properties of coagulation

A

Must remain local as surrounding cells must prevent accumulation of clotting

62
Q

Intrinsic coagulation

A

Triggered by factors within the blood/blood vessel

63
Q

Extrinsic coagulation

A

Triggered by factors outside the blood/blood vessel

64
Q

Contact activation or intrinsic pathway

A

Triggered by negatively charged surfaces
-Activated platelets
-Collagen

65
Q

Tissue factors or extrinisc pathway

A

Triggered by exposure to tissue factor or factor III-Significantly faster due to less reactions being needed

66
Q

Three phases of coagulation

A
  1. Prothrombin activator formation
  2. Prothrombin converted to enzyme thrombin
  3. Thrombin catalyzes fibrinogen–> fibrin
67
Q

Role of platelet-derived growth factor

A

Division of smooth muscle cells and fibroblasts to rebuild blood vessel outer walls

68
Q

Role of vascular endothelial growth factor

A

Restores endothelial lining

69
Q

Fibrinolysis

A

-Removes unneeded clots after healing
-Begins within 2 days and continues for several days

70
Q

Plasmin

A

Fibrin digesting enzyme
-Produced by activated plasminogen
-Trapped during clot formation causing a negative feedback loop

71
Q

Thrombus

A

Blood clot

72
Q

Embolus

A

Unattached mass that travels in the bloodstream

73
Q

Thrombocytopenia

A

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
Q

Reasons for an inability to synthesize procoagulants

A

-Impaired liver function
-Caused by vitamin K deficiency, hepatitis, and cirrhosis

75
Q

Hemophilia A

A

Factor VIII deficiency (77% of all cases)

76
Q

Hemophilia B

A

Factor IX deficiency

77
Q

Hemophilia C

A

Mild type; factor XI deficiency

78
Q

Disseminated intravascular coagulation

A

Widespread clotting of an intact vessel combined with severe bleeding

79
Q

Causes of disseminated intravascular coagulation

A

Usually pregnancy complications or incompatible blood transfusions that result in adverse reactions

80
Q

Reason for aspirin to not be instructed before surgery

A

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
Q

Life Span of Platelets

A

10 days

82
Q

Area of blood cell formation in bone marrow

A

Axial skeleton, girdles, and proximal epiphysis of humerus and femur.

83
Q

Reason to give children vitamin K shots

A

In order to have the means necessary to form clots an infant may not otherwise be able to heal

BSCI202: Anatomy & Physiology II (15 decks)

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