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Anatomy and Physiology > 40B - Lecture Chapter - #19 > Flashcards

40B - Lecture Chapter - #19 Flashcards

1
Q

Functions of blood

A
  1. Transportation
  2. Regulation
  3. Protection
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2
Q

Function of blood (transportation)

A
  1. Cells

2. Plasma

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3
Q

Function of blood (regulation)

A
  1. pH (buffers)
  2. Body temp
  3. Control water content
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4
Q

Function of blood (protection)

A
  1. Blood loss (clotting)
  2. Cells for defense (WBC / Leukocyte)
  3. Proteins that circulates in blood called anti-bodies
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5
Q

Physical characteristics of blood

A
  1. Thicker, sticky, and more viscous than water
  2. Temp is 1C higher than body temp
  3. pH is 7.35 - 7.45
  4. Volume of blood is ~5L
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6
Q

What is the pH of blood?

A

7.35 - 7.45

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7
Q

Acidosis

A
  • pH of blood is lower than 7.35
  • Decrease activity of CNS
  • Deadly below 7.0
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8
Q

Alkalosis

A
  • pH is higher than 7.45
  • Increase activity of CNS and PNS
  • Deadly above 7.65
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9
Q

What is the volume of blood?

A

~ 5L

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10
Q

Albumin

A
  • Transport Protein*
  • Made by liver
  • Transport hydrophobic molecules
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11
Q

Globulin

A
  • GENERAL TERM. IE: ENZYME*
  • Made by liver
  • Made by WBC
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12
Q

Immunoglobin

A 
AKA Antibody ( plasma protein)
-Body makes defense weapon
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13
Q

Fibrinogen

A
  • Specific globulin

- Helps with blood clotting

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14
Q

Other solutes in blood

A
  1. Electrolytes
  2. Nutrients
  3. Respiratory
  4. Waste product
  5. Regulatory substances
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15
Q

Regulatory substances in blood

A

Enzymes, hormones, vitamins

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16
Q

Formed elements in blood

A
  1. RBC
  2. WBC
  3. Platelets
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17
Q

Formed elements (RBC)

A
  • Make protein hemoglobin
  • Transport O2 and CO2
  • Disc shaped no nucleus
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18
Q

Formed elements (WBC)

A
  • Defense

- Lifespan varies

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19
Q

Formed elements (Platelets)

A

AKA thrombocytes

  • Blood clot
  • Lifespan ~ 1wk
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20
Q

WBC / Leukocytes

A
  1. Neutrophil
  2. Eosinophil
  3. Basophil
  4. Lymphocytes
  5. Monocyte
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21
Q

Neutrophil

A
  • First responder to tissue damage or bacterial infection
  • Able to leave blood stream and go into tissue
  • Destroy pathogen though phagocytosis
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22
Q

Eosinophil

A

-Release histamine-ase (anti-histamine)

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23
Q

Basophil

A
  • Release histamine

- Causes vasodilation

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24
Q

Vasodilation

A

Widening of blood vessels

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25
Q

Lymphocytes

A
  • T Cells: T-lymphocytes

- B Cells: B-lymphocytes

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26
Q

Monocyte

A
  • Enter tissue and differentiate into macrophages
  • Macrophage found in spleen and liver
  • Recycling of old RBC
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27
Q

Hematocrit

A

Percent of RBC in whole blood

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28
Q

Average hematocrit

A

~45%

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29
Q

Why is do males have a higher hematocrit than females?

A

Testosterone increases EPO

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30
Q

EPO

A

Erythropoietin

  • Made by kidney
  • Main function is to increase RBC production
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31
Q

Anemia

A

Lower than normal hematocrit

~Lower than 30%

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32
Q

Polycythemia

A

Higher than normal hematocrit

~Higher than 65%

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33
Q

Causes of anemia

A
  • Decease EPO
  • Low iron in diet
  • Decease B12
  • Blood loss
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34
Q

Causes of polycythemia

A
  • Tissue hypoxia
  • Dehydration
  • EPO is administered when person has kidney disease
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35
Q

Hypoxia

A

Decrease O2 in tissue

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36
Q

What happens when one artificially induces polycythemia?

A
  • Increase O2 capacity
  • Increase viscosity
  • Increase BP
  • Increase formation of blood clot
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37
Q

Hemopoiesis

A

AKA hematopoiesis

Process to make all blood cells

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38
Q

Where do RBC form and go after formed?

A

All RBC cells start with stem cells at RBM and then go into blood vessel

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39
Q

Which cells can exit blood stream and enter tissue?

A

White Blood Cells

Ex: goes in to lymph nodes

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40
Q

What specific WBC can go into tissue?

A
  1. Macrophage (from monocyte)

2. Plasma cell (from B-Lymphocyte)

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41
Q

Symptoms of Acidosis

42
Q

Symptoms of Alkalosis

A

pH > 7.65

Convulsions, hyperventilation, vomiting

43
Q

RBC formation

A

Proerythroblast -> Reticulocyte -> Erthrocyte

44
Q

Platelet formation

A

Megakaroblast -> Megakaryocyte -> Thrombocyte

45
Q

Hemoglobin molecule

A

Heme group - O2

Protein Component - CO2

46
Q

Carbon Monoxide affect on hemegroup

A

CO has a stronger attachment to Hemegroup than O2

47
Q

Lifespan of RBC

A

~4mo (120 days)

48
Q

Where does RBC recycle?

A

Liver, bone marrow, spleen

49
Q

Steps for globin to recycle

A
  1. Amino acids get reused for protein synthesis
50
Q

Steps for hemegroup (Fe+3)

A
  1. (BV) Keep iron
  2. (BV) Transferrin picks up
  3. (BV) Inside liver and binds to Ferritin
  4. (BV) Fe+3 attach to transferrin and bring to RBM
  5. (BV) Erythropoiesis in RBC
  6. (BV) Back to blood stream
51
Q

Steps for hemegroup (Biliverdin)

A
  1. Converts into Bilirubin
  2. (BV) Goes into liver
  3. (BI) Goes into bile and small intestine
  4. Either goes to feces or urine
52
Q

Jaundice

A

Build up of bilirubin in blood, molecule will enter sclera and skin

53
Q

Jaundice in newborn

A

Liver not mature enough to handle recycling of RBC

Treatment: Blue or fluorescent light. Breaks down Bilirubin

54
Q

Jaundice in adults

A

Liver disease is the usual cause

55
Q

Emigration of WBC

A

Neutrophil -> Rolling -> Sticking -> Squeezing

56
Q

Hemorrage

A

Loss of large amount of blood from blood vessel

57
Q

Blood doping

A

Artificially inducing polycythemia (Usually to gain a competitive edge)

58
Q

Hemostasis

A

Sequence of responses that stops bleeding

3 mechanisms

59
Q

3 Mechanisms for Hemostasis

A
  1. Vascular spam
  2. Platelet plug formation
  3. Blood clotting
60
Q

Vascular spams (Hemostasis)

A

Contraction of smooth muscle in all of blood vessels

61
Q

Platelet Plug formation (Hemostasis)

A

Sticky substance. Changes shape and platelets will release chemicals. Platelets will make a clump

62
Q

Blood clotting (Hemostasis)

A

Needs to make sticky protein and fibrinthread

63
Q

Blood clotting cascade

A
  1. Extrinsic Pathway

2. Intrinsic pathway

64
Q

Extrinsic pathway

A

Appropriate

*Tissue trauma -> Tissue factor -> Blood vessel -> Prothrombinase

65
Q

Intrinsic pathway

A

Inappropriate

*Blood trauma -> damaged endothelial and damaged platelet -> Prothrombinase

66
Q

What enzyme is needed for prothrombin to make thrombin

A

Prothrombinase

67
Q

Prothrombin

A

Made by liver, requires K+

Inactive and soluble

68
Q

Thrombin

A

Activated

Enzyme

69
Q

What is enzyme is needed to make Fibrinogen to make Firbin

70
Q

Fibrinogen

A

Plasma protein made by liver

Soluble and inactive

71
Q

Fibrin

A

Insoluble, protein, sticky, major form of clot

72
Q

Thrombolytic Agents

A

AKA Fibrinolysis (plasminogen)

73
Q

What chemicals can make Fibrinolysis into Plasmin

A
  1. Streptokinease (bacterial)

2. TPA (tissue plasminogen activator) (human)

74
Q

Plasmin

A

AKA fibrinolysin

-Goes after fibrin and breaks it down

75
Q

Anticoagulants

A

Stop fibrin formation or stops blood clotting

76
Q

Coumadin

A

Anticoagulant. Warfaren. Medicine
Decrease in Vit K in body
Liver -> (VIT K IS DECREASED) -> Prothrombin -> Thrombin

77
Q

Heparin

A

Bind to anti-thrombin and increase effectiveness, body makes

Prothrombin (KNOCKS OUT) -> Thrombin

78
Q

Asprin

A

Inhibit platelet activation, prevents platelets to becoming sticky

79
Q

Intravascular Clotting

A

*Inappropriate clot

Cause: Blood trauma

80
Q

Causes of intravascular clotting

A
  1. Roughening endothelium lining of blood vessels

2. Cause blood to slow down in atherosclerosis

81
Q

Atherosclerosis

A

Narrows leumen, concentration of activated platelets and blood clots form

82
Q

Thrombosis

A

Clotting in unbroken blood vessel

83
Q

Thrombus

84
Q

Embolus

A

Clot that moves in blood vessel

85
Q

Pulmonary Embolism

A

Clot that blocks pulmonary arteries and arterioles

86
Q

Symptoms of pulmonary embolism

A
  1. Sudden and unexplained shortness of breath
  2. Chest pain
  3. Cough
87
Q

Treatment for pulmonary embolism

A
  1. Treat with anti-coagulent

2. Treat with Thrombolytic agents

88
Q

Hemophila

A
  • Bleeding disorder
  • Lacks clotting factor
  • Inherited deficiency or may occur spontaneously
89
Q

Treatment to hemophila

A
  1. Administer missing clotting factor

2. Drug that increase blood clotting factor

90
Q

Leukemia

A

*White blood cell

More WBC than RBC, group of RBM cancers

91
Q

Characteristics of leukemia

A
  1. Increase in abnormal WBC that multiply uncontrollably
  2. Causes hypoxia
  3. Abnormal blood clotting
  4. Susceptible to infection
  5. Cancer can spread to spleen, liver, lymph nodes
  6. Anemia
92
Q

Acute Anemia

A

Associated with children and sometimes in adults. Symptoms develop rapidly

93
Q

Chronic Anemia

A

Associated with adults. Symptoms may take years

94
Q

Causes of leukemia

95
Q

Risk factors for leukemia

A
  1. Genetics
  2. Radiation
  3. Environmental
  4. Microbes
96
Q

Treatment for leukemia

A
  1. Chemo (need RBM transplant)

2. Blood transfusion

97
Q

Sickle Cell Disease

A

Inherited disease in which the RBC forms and abnormal shape because the hemoglobin molecule inside cell changes

98
Q

What is the adaptive advantage to having malaria and sickle cell?

A

The parasite in Malaria will be killed if it enters sickled cell

99
Q

Characteristics of Sickle Cell Anemia

A
  1. RBC die quickly. Tissues do not get O2
  2. Increase hemoglobin in blood, damage filtration in Kidney
  3. Increase tendency for blood clotting
100
Q

Symptoms of Sickle Cell Anemia

A
  1. Anemia
  2. Jaundice
  3. Pain (clogging capillaries)
  4. Shortness of breath
101
Q

Treatment of Sickle cell Anemia

A
  1. EPO
  2. Pain
  3. Bone marrow transplant
  4. Blood transfusions
  5. Hydroxy Urea
102
Q

Hydroxy Urea

A

Increase form of Hb-F

Decrease incidence RBC to sickle

Anatomy and Physiology (22 decks)

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