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Physiology > Cardiovascular Physiology 5 Blood and Hemostasis > Flashcards

Cardiovascular Physiology 5 Blood and Hemostasis Flashcards

1
Q

what is the total blood volume in men and women

A

-men - 5L
-women- 4L
-about 7% body weight

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2
Q

what are the components of blood

A

-cellular elements
-plasma

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3
Q

what does the cellular elements include and how much of the blood does it make up

A

~45%
-blood cells- RBCs, WBCs, and platelets

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4
Q

what is in the plasma and how much of the blood does it make up

A

~55%
-92% water
-7% plasma proteins
-1% dissolved substances such as organic molecules, ions, trace elements, vitamins, dissolved gases

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5
Q

what are the functions of blood

A
  • supplies nutrients and O2
  • removes waste products and CO2
  • carries regulatory factors (hormones)
  • defends against infection (immune function)
  • hemostasis (keeping blood in blood vessels)
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6
Q

what makes plasma proteins and what are the types

A

liver
-albumins
-globulins
- fibrinogen

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7
Q

what do albumins do

A

main determinant of Pi C

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8
Q

what do globulins do

A

antibodies

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9
Q

what do fibrinogens do

A

clotting proteins, zymogens

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10
Q

what are the functions of plasma proteins

A

-maintain Pi C
-transport proteins for lipids (steroids)
- hormones
-extracellular enzymes
-immunity
-blood clotting

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11
Q

what is serum

A

plasma - clotting proteins

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12
Q

what do erythrocytes do

A

transport O2 and CO2

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13
Q

what do leukocytes do

A

body defense

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14
Q

what do thrombocytes (platelets) do

A

hemostasis

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15
Q

what is hematocrit

A

percentage of total blood volume occupied by blood cells

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16
Q

what is the normal hematocrit for men and women

A

45%

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17
Q

what will hematocrit do to resistance, flow rate, and turbulent flow

A

-resistance: increase
-flow rate: decrease
-turbulent flow: decrease

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18
Q

what is hematopoiesis

A

blood cell production

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19
Q

where does hematopoiesis occur

A

red bone marrow- spongy bone

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20
Q

what are all formed elements (myeloid and lymphoid) produced from

A

pluripotent hematopoietic stem cell

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21
Q

what differentiates from a myeloid stem cell

A

erythrocyte
neutrophil
monocyte
eosinophil
basophil
megakaryocyte -> platelets

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22
Q

what is the control factor for erythrocytes

A

erythropoietin

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23
Q

what is the control for leukocytes

A

CSFs and ILs

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24
Q

what is the control for thrombocytes

A

thrombopoietin

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25
Q

what do RBCs NOT contain

A

-no nucleus or organelles
-no DNA
-no centrioles

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26
Q

what are the enzymes in RBCs

A

-glycolytic enzymes for glycolysis
-carbonic anhydrase

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27
Q

how many hemoglobin molecules are there per RBC

A

2x10^8/ RBC

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28
Q

what filters RBCs

A

spleen and the liver

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29
Q

where is erythropoietin made

A

kidney

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30
Q

what factors cause hypoxia and thus stimulate erythropoietin

A

-low blood volume
-anemia
-low Hb
-poor blood flow
- pulmonary disease
-high altitude

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31
Q

what is the pathway of erythropoietin action

A

kidney -> makes erythropoietin -> hematopoietic stem cells ->proerythroblasts -> red blood cells -> tissue oxygenation

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32
Q

what are reticulocytes

A

young RBCs

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33
Q

what percentage of circulating RBCs do reticulocytes make up

A

1%

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34
Q

when do levels of reticulocytes increase

A

during periods of rapid RBC production

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35
Q

what does RBC production require

A

-iron
-folic acid
-vitamin B12

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36
Q

what is the normal Hb content of blood in men and women

A

men: 13-18 g/dL
women: 12-16 gram/dL

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37
Q

what is folic acid necessary for

A

DNA replication and cell division

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38
Q

what is vitmain B12 necessary for

A

DNA replication and cell division

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39
Q

what is a result of vitamin B12 deficiency

A

pernicious anemia

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40
Q

what happens when hemoglobin gets broken down

A

-globin is made into AA’s
-heme is broken down into iron which gets recycled and stored as ferritin in the liver and bile pigments that are secreted into small intestine and excreted through the feces

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41
Q

what bile pigments are formed when RBCs are broken down

A

bilirubin and biliverdin

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42
Q

what is iron deficiency

A

Hb deficiency

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43
Q

what is hemochromatosis and effects

A

-too much iron
- damages liver, heart, pituitary gland, pancreas and joints

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44
Q

what do patients with chronic renal failure have to little of

A

erthyropoietin and require administration of synthesis forms to maintain normal RBC

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45
Q

what can happen to atheletes who misuse RBC synthetic form

A

can die from polycythemia bc increased RBC -> increases viscocity of blood -> increases resistance -> decreased blood flow and results in clotting, stroke, and heart failure

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46
Q

why do men have a higher hematocrit than women

A

testosterone enhances RBC production by increasing EPO

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47
Q

what is the definition of anemia

A

decrease in the O2 carrying capacity of blood by decrease in number of RBCs and or/ in Hb concentration

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48
Q

what is hemorrhagic anemia and cause

A

decrease in O2 carrying capacity due to bleeding

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49
Q

what is hemolytic anemia and cause

A

destruction of RBC due to malaria and/or sickle cell anemia

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50
Q

what is aplastic anemia and cause

A

bone marrow cannot perform erythropoiesis/hematopoiesis due to a bone marrow defect

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51
Q

what is renal anemia caused by

A

kidney disease

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52
Q

what is polycythemia defined by

A

hematocrit greater than 60%

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53
Q

what are the two types of polycythemia

A

-polycythemia vera
- secondary polycythemia

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54
Q

what is the cause of polycythemia vera

A

genetic condition that over produces RBCs

55
Q

what is the cause of secondary polycythemia and effects

A

cause: hypoxia/high altitude
can cause heart failure

56
Q

what are antigens on RBCs called

A

agglutinogens

57
Q

most antigens on RBC are ____

A

relatively weak

58
Q

what antigens on the RBC membrane is blood typing based on

A

A, B and Rh

59
Q

what is the presence or absence of A and B antigens determined by genetically

A

incomplete dominance

60
Q

what is the presence or absence of Rh antigens determined by genetically

A

mendelian genetics

61
Q

when do antibodies to A/B antigens on RBCs appear

A

2-8 months after birth, NOT AFTER AN EXPOSURE

62
Q

how are antibodies to A/B antigens introduced to immune system

A

through food and bacteria

63
Q

when is maximum titer of antibodies to A/B antigens

A

10 years then declines with age

64
Q

what happens when inappropriate A-B-O blood is transfused

A

agglutination

65
Q

what does agglutination cause

A

obstruction of small blood vessels

66
Q

what happens hour to days after agglutination and what is cause

A

hemolysis occurs due to extreme distortion of RBCs and action of phagocytic WBCs

67
Q

what can the pathologic effects of agglutination do

A

can be extreme and fatal

68
Q

what is blood transfusion made of

A

not whole blood, but packed RBCs

69
Q

what is the reaction to worry about in blood transfusions

A

recipients plasma and donor’s RBCs

70
Q

what blood type is universal donor? universal recipient?

A

donor: O-
recipient: AB+

71
Q

are there Rh antibodies in the blood?

A

no only if the person has been exposed

72
Q

what happens if an Rh- person is exposed to Rh+ blood

A

may see mild agglutination response 2-4 weeks after exposure but first exposure is usually mild

73
Q

what is erythroblastosis fetalis

A

Rh negative mother, Rh positive fetus

74
Q

what happens in the first and second pregnancies in erythroblastosis fetalis

A

first: fetal red cells leak into maternal circulation during labor. mother develops anti-Rh antibodies. low risk to fetus because it occurs late in pregnancy
second: maternal IgG crosses placenta and destroys fetal RBCs

75
Q

what is the treatment for erythroblastosis fetalis

A

administration of anti-RhD immunoglobulin (RhoGAM) after delivery

76
Q

what are platelets derived from

A

megakaryocytes

77
Q

what is the lifespan of platelets

A

10 days

78
Q

what is the primary role of platelets

A

hemostasis- keeping blood in blood vessel

79
Q

do platelets have nuclei and can they divide

A

no and no

80
Q

what do platelets contain

A
  • actin and myosin
    -enzymes and organelles for aerobic CR
  • enzymes for prostaglandin synthesis
  • fibrin-stabilizing factor
    -growth factors that stimulate endothelial cell, VSM, and fibroblasts to divide and grow
81
Q

what are the 4 steps of hemostasis

A
  1. formation of platelet plug to block hole in damaged vessel
  2. vasoconstriction of damaged vessel to decrease blood flow and pressure
  3. clot formation
  4. clot dissolution
82
Q

what are the steps leading to platelet plug and vasoconstriction

A

-platelets stick to damaged endothelial surface via Von Willebrand Factor
-platelets release contents of secretory vesicles
-stimulate production of thromboxane A2 from platelet plasma membrane

83
Q

where do NSAIDs work

A

at the cyclooxygenase pathway

84
Q

where do steroidal anti-inflammatory drugs like prednisone work

A

phospholipid -> arachidonic acid

85
Q

what limits aggregation and activation of the platelet plug

A

NO and PGI2

86
Q

what stimulates aggregation and activation of the platelet plug

A

TXA2

87
Q

what is the definition of coagulation

A

blood converted into solid gel called clot or thrombus

88
Q

where does clotting occur

A

around platelet plug

89
Q

what is the function of a blood clot

A

to support and reinforce platelet plug

90
Q

what is prothrombin activator and what does it do

A

it is a complex of Xa/Va and it activates prothrombin into thrombin

91
Q

what does thrombin do

A

activates factor 13 which acts with fibrinogen to make stabilized fibrin

92
Q

when is the intrinsic pathway activated

A

trauma to blood
-blood comes in contact with collagen from traumatized blood vessel wall

93
Q

where are all the required factors for the intrinsic factors located

A

within the blood

94
Q

which pathway is faster

A

extrinsic

95
Q

when is the extrinsic pathway activated

A

trauma to vascular
trauma to surrounding extravascular tissue

96
Q

what does the extrinsic pathway require

A

tissue factor (thromboplastin) produced by cells located outside of endothelial cells

97
Q

what do instrinsic and extrinsic pathways both make

A

prothrombin activator

98
Q

what does thrombus formation begin with

A

extrinsic pathway followed by intrinsic activation by thrombin

99
Q

what ion is required for the clotting cascade

A

Ca2+

100
Q

what is the required cofactor for enzyme IXa

A

factor 8

101
Q

what are the 2 types of hemophilia, incidence rate and what factor do each not have

A

-hemophilia A- 90%- missing factor 8
-hemophilia B - 10%- missing factor 9

102
Q

what does the liver need to produce zymogens

A

vitamin K

103
Q

what is the role of the liver in making clotting factors

A

synthesizes bile salts -> bile salts in bile -> Gi tract absorbs vitamin K -> vitamin K in blood -> synthesizes clotting factors -> clotting factors in blood (zymogens)

104
Q

why is it important to limit clot formation

A

prevent thrombus from spreading

105
Q

what are the 3 things that limit clot formation

A

-tissue factor pathway inhibitor (secreted by endothelial cells)
- thrombomodulin causes activated protein C and inhibits factor 8a and 5a
-antithrombin III plasma protein inhibits thrombin

106
Q

what are the steps in fibrinolysis

A

-the plasma protein plasminogen is trapped in a clot just like other plasma proteins
- injured tissues and endothelial cells slowly release tissue plasminogen factor (t-PA)
-t-PA converts plasminogen to plasmin a few days after clot is formed
-plasmin digests fibrin fibers, fibrinogen, prothrombin, and factors 5,8, and 12

107
Q

what is a thrombus

A

a clot that forms and persists in an unbroken blood vessel

108
Q

what can a thrombus lead to

A

can block the vessel, lead to ischemia, and tissue death downstream from the cloth

109
Q

what is an embolus and what can it do

A

a free floating object in the blood stream, can wedge and occlude a vessel

110
Q

what does pulmonary embolism do

A

impair oxygenation

111
Q

what does a cerebral embolism do

A

cause strokes

112
Q

what do low doses of aspirin do vs high doses

A

low: inhibit formation of thromboxane A2 by platelets but not prostacyclin by endothelium
high: inhibit formation of prostacyclin

113
Q

what are the anticoagulants

A

-asprin
- heparin
- recombinant t-PA
-warfarin
-pradaxa
-plavix

114
Q

what does heparin do

A

binds to antithrombin III and increases its activity by 100-1000x

115
Q

what does recombinant t-PA do

A

dissolve intravascular clots if given immediately

116
Q

what does warfarin do

A

blocks vitamin K

117
Q

what does pradaxa do

A

blocks active site of thrombin

118
Q

what does plavix do

A

blocks platelet activation

119
Q

what is thrombocytopenia

A

a lack of platelets that causes spontaneous bleeding in small vessels even in normal movement

120
Q

what causes thrombocytopenia

A

anything that affects bone marrow

121
Q

what is the treatment for thrombocytopenia

A

platelet transfusion

122
Q

how is liver disease a bleeding disorder

A

causes a lack of zymogens

123
Q

what could cirrhosis and hepatitis require for treatment

A

tranfusions

124
Q

what causes von willebrand disease and what happens

A

reduced levels of vWf
decreases platelet plug formation

125
Q

what happens in vitamin K deficiencies

A

decreased synthesis of clotting factors

126
Q

what are the 2 tests that assess coagulation and what do they each assess

A

-activation partial thromboplastin time (PTT/aPTT): assesses intrinsic pathway
-prothrombin time (PT): assesses extrinsic pathway

127
Q

what is citrate used for in coagulation tests

A

prevents blood from clotting

128
Q

what is a normal PTT

A

22-39 seconds

129
Q

what is a normal PT

A

11-15 seconds

130
Q

what is the formula for INR

A

PT patient/PT normal

131
Q

what is a normal INR

A

less than 1.1

132
Q

what does INR of 2-4 mean

A

-blood clots 2-4 times slower than normal
-effective therapeutic range
-OK for dental work

133
Q

what does an INR of over 4 mean

A

risk of bleeding to great
-work with physician

Physiology (41 decks)

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