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Anatomy Spring semester > Chapter 17 Blood > Flashcards

Chapter 17 Blood Flashcards

1
Q

What are the three blood functions?

A
  1. Transport
  2. Maintenance
  3. Protection
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2
Q

Blood functions

Transport

A
  • Oxygen and nutrient delivery to tissues (glucose, amino acids, lipids, etc)
  • Waste removal from tissues (CO2)
  • hormone transport to target organs (hormones go directly to bloodstream)
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3
Q

Blood functions

Maintenance

A
  • body temperature (any fluid body produces will be mostly water and water absorbs heat)
  • pH (buffer- reduced bug changes in blood)
  • Fluid volume
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4
Q

Blood functions

Protection

A
  • blood clotting (cutting, scraping skin)
  • infection (immune system function, WBC)
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5
Q

Characteristics of blood

A
  • Scarlett to dark red in color (color is determined by how much oxygen is present)
  • brighter red= more oxygen blood
  • dark red=less oxygen blood
  • Total amount= 5.25 L
  • pH range= 7.35-7.45
  • Viscous due to erythrocytes (blood is thicker than water)
  • Erythrocytes are RBCs- more RBCs in blood means the blood will be more thicker
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6
Q

Blood composition: plasma and blood cells

Blood plasma

A
  • fluid (non-living) portion of blood
  • Composition is 90% water and 6 solutes found in plasma
    1. Electrolytes Greatest amount
    2. Nitrogenous substances (urea, uric acid, etc)
    3. Organic nutrients (glucose, amino acids, triglycerides, etc)
    4. Respiratory gases (oxygen and carbon dioxide)
    5. Hormones
    6. Plasma proteins most of mass (produced by liver)
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7
Q

Plasma proteins

What are the several types of plasma proteins

A
  1. Albumin
  2. Fibrinogen
  3. Globulins
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8
Q

Plasma protein

Albumin

A
  • Major transport protein of blood and contributes to osmotic pressure in capillaries (antibodies)
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9
Q

plasma protein

Fibrinogen

A
  • soluble protein that functions in blood clotting
  • blood is only fluid tissue, you cannot see fibrinogen bc it is dissolved in blood–> you can only see it in an injury
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10
Q

plasma protein

globulins

A
  • Transport proteins, antibodies (immune defense) etc
  • contributes to osmotic pressure in our capillaries
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11
Q

blood cells

A
  • All blood cells are short lived and non mitotic
  • red bone marrow pumps out blood cells to keep up with what you are losing
  • three types of blood cells
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12
Q

What are the three types of blood cells

A
  1. Erythrocytes
    -Red blood cells
    -Hematocrit: portion of total blood volume made up by erythrocytes
    -males: -47%
    -females: - 42%
  2. leukocytes (White blood cells)
  3. Thrombocyte (platelets) important for blood clotting
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13
Q

Hematopoiesis

A
  • Production of blood cells (all 3 types)
  • occurs only in red bone marrow
  • all blood cells arise from Hematopoietic stem cell (stem cell can become anything at first)
  • Hematopoietic stem cells eventually become “committed” to forming a certain type of blood cell
  • Once committed, the cell cannot become any other cell type
  • In a single day-marrow creates- 100 billion new cells
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14
Q

Erythrocytes (RBCS)

Erythrocytes

A
  • blood cell type responsible for respiratory gas transport
  • Nuclei and organelles removed during cell development (makes more room for extra hemoglobin)
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15
Q

Erythrocytes

Hemoglobin (Hb)

A
  • Protein responsible for O2 transport in blood
  • hemoglobin composed of heme pigment bound to globin protein
  • globin protein has 2 alpha chains, 2 beta chains
  • each chain binds to 1 heme group
  • each heme group has Fe+ ion at center
  • Each Fe+ can bind one molecule O2
  • Hb binds and breaks free of oxygen very easily
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16
Q

Erythrocytes

Why are Erythrocytes are ideal for gas exchange

A
  1. large surface area relative to volume (to bring or leave smth in cell, you need to go through the plasma membrane. The more plasma membrane then it is easier to cross)
  2. Flattened disc shape
  3. Anaerobic mechanism of energy production (RBCS do not use any of the oxygen then carry-no oxygen wasted by the RBCs. RBCs are gonna use glycolysis to produce any ATP they need)
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17
Q

Erythropoiesis

A
  • Erythropoiesis: The production of red blood cells
  • Hematopoietic stem cell “commits” to a Proerythroblast
  • Tightly regulated process
  • When there are too few erythrocytes it is known as Hypoxia
  • too many erythrocytes leads to cardiovascular issues and it is hard to pump blood
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18
Q

Erythropoiesis (hormonal controls)

Erythropoietin (EPO)

A
  • EPO: stimulates erythrocyte Production
  • produced and released by kidneys
  • kidneys have a baseline of how much EPO they produce, if kidney cells become hypoxic (short on oxygen) it stimulates EPO release
  • EPO only stimulates cells already committed to becoming erythrocytes
  • Small amount almost always present in blood to set basal rate production
  • (-) feedback mechanism: excessive oxygen supply suppresses EPO release
  • directly stimulates
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19
Q

Erythropoiesis (hormonal controls)

Testosterone

A
  • enhances production of EPO
  • males generally have more erythrocytes and Hb than females
  • indirectly
  • more testosterone–> more EPO
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20
Q

Erythropoiesis

Dietary needs for normal erythrocyte production:

A
  • General nutrients: amino acids, lipids, carbohydrates necessary for cell synthesis
  • B-complex vitamins: B12 and folic acid
    -Necessary for normal DNA synthesis
  • Iron: Normal Hb synthesis
    -65% of bodys iron supply is in Hb (hemoglobin)
    -Remainder stored in liver, spleen, etc
    -“free” Iron bound to protein transferrin- erythrocyte takes up Iron as needed
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21
Q

Destroying Erythrocytes

A
  • Average lifespan: 120 days
    -Hb begins to degenerate, cell becomes less flexible
  • Macrophages engulf and destroy cell
    -heme group splits free from globin protein
    -heme broken down to bilirubin in the liver and excreted to intestines in bile–>leaves body in feces
    -Heme cannot be reused
    -Globin broken down to amino acids, released to circulation
  • Fe2+ bound to transport protein and saved for reuse
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22
Q

Homeostatic imbalances of Erythrocytes

Anemia

A
  • insufficient oxygen supply to meet body needs
  • Symptoms: paleness, old, short of breath, tired
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23
Q

Homeostatic imbalances of Erythrocytes

What is anemia caused by?

A

1. blood loss
-acute hemorrhagic anemia: severe, swift blood loss
-chronic hemorrhagic anemia: slow, persistent blood loss
2. Inadequate erythrocyte production
-Example: iron deficiency anemia (nutritional origins), renal anemia (little/no EPO release)
3. Excessive erythrocyte destruction/deformation
-sickle cell anemia

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24
Q

Homeostatic Imbalances of Erythrocytes

Polycythemia

A
  • increase in number of erythrocytes
  • icrease viscosity (thickness)
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25
Q

what are the three types of polycythemia?

A
  1. Polycythemia vera
  2. secondary polycythemia
  3. Blood doping
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26
Q

homeostatic imbalances of Erythrocytes

polycythemia vera

A
  • bone marrow cancer
  • hematocrit levels -80%
  • effect: blood volume doubles, vascular system engorges with blood and impairs circulation
  • treatment: therapeutic phlebotomy
27
Q

homeostatic imbalances of Erythrocytes

secondary polycythemia

A
  • increase EPO release, low oxygen availabilty
  • caused by high altitude living, smoking, etc
28
Q

homeostatic imbalances of Erythrocytes

Blood doping

A
  • temporary polycythemia: synthetic EPO/oxygen carries, blood transfusions (doing it to themselves)
  • Used by athletes to increase oxygen carrying capacity during athletic events
  • risks: stroke, heart failure
29
Q

Blood typing and blood transfusions

Body compensates for blood loss 2 ways:

A
  1. decreasing blood volume to injured blood vessels
  2. increasing red blood cell production by red bone marrow
30
Q

blood typing and blood transfusions

The body can only compensate so much

A
  • losing 15-30% total blood volume leads to weakness, 30%+ loss leads to severe shock (possible death)
  • Whole body transfusions are rare…only necessary when large volumes of blood are lost. More often, red cell transfusions are used
31
Q

Blood transfusions: blood groups

Erythrocytes have very specific extracellular markers called….

A

ANTIGENS (A, B,O antigens)
* transfusions between two people with different antigens usually cannot occur. The immune system will attack the “mismatches” blood cells
* medical field is mostly concerned with ABO Blood groups and Rh blood groups

32
Q

ABO blood groups

1. Blood type A: cells have……. antigen
2. Blood type B: cells have……. antigen
3. Blood type O: cells have……. antigen
4. Blood type AB: cells have……. antigen

A
  1. cells have “A” antigen
  2. cells have “B” antigen
  3. cells do not have any antigen
  4. cells have both “A” and “B” antigen
33
Q

Blood groups

Immune system antibodies that will attack mismatched blood cells

A

Agglutinins

34
Q

Agglutinins

  1. Person with Type A blood has….
  2. Person with Type B blood has…
  3. Person with Type AB blood has..
  4. Person with Type O blood has…
A
  1. Person with Type A blood has anti-B antibodies (agglutinins)
  2. Person with Type B blood has anti-A antibodies (agglutinins)
  3. Person with Type AB blood has neither type of antibody
  4. Person with Type O blood has both anti-A and anti-B antibodies
35
Q

Blood groups

Rh Blood groups

A
  • Five antigens make up this blood groups–> C,D,E,c and e
36
Q

Rh blood group

If you carry the D anitgen you are?

A

Rh+

37
Q

Rh blood group

If you carry the C,E,c or e antigen you are?

A

Rh-

38
Q

Rules for Rh +/- donation?

A
  • Rh- can only recieve - blood (produces antibodies)
  • Rh+ can receive + or - blood
39
Q

Blood transfusions

Transfusion reaction

A
  • Mismatching blood type leads to transfusion reactions
  • antibodies attack “foreign” donor blood cells (don’t belong)
  • Foreign erythrocytes are clumped together via agglutination--> blocking blood vessels
  • “foreign” blood cells will eventually start to lyse-release hemoglobin to blood stream. This results in decrease oxygen transport, hemoglobin passes freely into kidney tubules–> kidney shutdown
  • Ex: blood type A cannot donate to blood type B
40
Q

Blood Transfusions: Transfusion reactions

Type O

A

”universal donor”
* Neither antigen is present on blood cell surface
* Agglutinins in recipient body have no basis to judge “matched” vs. “mismatched”
* Problem: Type O has both types of agglutinins**

41
Q

Blood Transfusions: Transfusion reactions

Type AB

A

“universal recipient”
* Neither antibody is present
* Nothing to attack “foreign” red blood cells

42
Q

Leukocytes (WBCs)

A
  • Function: responsible for defending the body
43
Q

Characteristics of leukocytes

A
  1. not restricted to the blood vessels
    -use vessels as transport to various parts of the body
    -can leave vessels via capillary walls to reach source of infection. This is important because it can destory the infection earlier on before it reaches cardiovascular system
  2. Can be produced very quickly
    -number in body can double within 2-3 hours to help destroy infection quickly
  3. Average lifespan: 13-20 days
    -if WBC is not used it lasts the full 20 days
    -if WBC is used it doesn’t last as long
  4. two major categories: granulocytes and agranulocytes
44
Q

Leukocytes

Granulocytes

A
  • spherical in shape, large and packed with granules
45
Q

What are the types of granulocytes?

A
  1. neutrophils
  2. Eosinophils
  3. Basophils
46
Q

Granulocytes

Neutrophils

A
  • “bacteria Killer”
  • 50-70% of total leukocyte population
  • granules contain defensins-antimicrobial protein. This kills off bacteria by punching holes in membrane. Neutrophil releases defensins which poke holes which leads to water going into the bacteria allowing the bacteria to become a “water ballon” and pop. It won’t cause infection anymore
  • chemically attracted to sites of inflammation
  • can become phagocytic (if bacteria is large in size and wants to get rid of it fast)
47
Q

Granulocytes

Eosinophils

A
  • Parasite killer”
  • 2-4% of leukocyte population
  • lysosomes in cell contain digestive enzymes
  • do not have enzymes that kills bacteria
  • digestive enzymes released will digest body wall of parasitic worms
48
Q

Granulocytes

Basophils

A
  • 0.5-1% of leukocyte population
  • have histamine-containing granules
  • histamine release causes vasodilation and attracts other leukocytes to area
  • blood vessels dilate due to histamine which allows them to transport basophils to infection quickly
  • more WBCS to infection site=more likely to be destroyed
49
Q

Leukocytes

Agranulocytes

A

leukocytes that lack visible granules

50
Q

Leukocytes

two types of agranulocytes

A
  1. lymphocytes
  2. monocytes
51
Q

Agranulocytes

lymphocytes

A
  • 25% of leukocyte population
  • migrate into and out of blood continuously
  • 3 types
    1. T-lymphocytes (T-cells): act against virus-infected cells and tumor cells (One T cell looks for one virus) (more specific)
    2. B-lymphocytes (B-cells): produce antibodies released to blood (antibodies are basically flags)
    3. Natural Killer (NK) cells: target cancerous cells & cells infected by virus
52
Q

Agranulocytes

monocytes

A
  • 3-8% of leukocyte population
  • Sit around until exposed to smth that doesn’t belong—> differentiate and form macrophages—> wondering around in body tissue destroying whatever needs to be destroyed
  • Differentiate into macrophages as they leave bloodstream & enter tissue
  • Actively phagocytic–> destroy bacteria, viruses, sources of chronic infection
53
Q

Leukopoiesis

A
  • production of leukocytes
  • stimulated by 2 chemical messengers
    1. interleukins
    2. colony stimulating factors
  • leukocyte differentiation
  • hematopoietic stem cell can form either
    1. myeloid stem cell: commits to either myeloblast or monoblast
    2. lymphoid stem cell: commits to either B-lymphocyte or T-lymphocyte precursor cells
54
Q

Homeostatic imbalances of leukocytes

Leukemia

A
  • Cancer resulting in over production of abnormal leukocytes(WBCs)
  • Extra” cells originate from single abnormal cell (doesn’t respond to infection or virus, therefore people with leukemia are much more prone to infection. A common cold can potentially be deadly)
  • Abnormal leukocytes remain unspecialized, proliferate extensively
  • Cancerous leukocytes crowd red marrow & immature leukocytes flood bloodstream
  • Other blood cell types are crowded out of blood, resulting in anemia & bleeding problem (cant form blood clots
  • Do not defend the body as they shouldinfection & hemorrhage occurs
55
Q

Homeostatic Imbalances of Leukocytes: Leukemia

Leukemia named according to how fast cells proliferate and the type of cell involved

A

Rate of proliferation:
A) Acute leukemia: derived from stem cells
Primarily affects children (also adults)
Is this development fast or slow? Fast bc the abnormal cells are stem cells

B) Chronic leukemia: derived from later cell stages
Primarily affects the elderly
Is this development fast or slow? Slow bc the abnormal cells arrive from a later cell stage

Type of cell involved:
A) Myeloid leukemia: involves myeloid stem cell descendants

B) Lymphocyte leukemia: involves lymphocytes

56
Q

Thrombocytes (platelets)

A
  1. Fragments of large cells (megakaryocytes)
    Megakaryocyte is fragmented into smaller platelet “cells”–> released to blood
  2. Average lifespan: only about 10 days if unused
    Blood platelets are shortest lived. If used it is shorter than 10 days
  3. Function: Initiate blood clot formation after damage to blood vessel wall
    When blood vessel wall is damaged/tornplatelets stick to each other & to injury site
    What effect does this have? Form a wall and temporary seal off where the damage is
    When no damage–>prostacyclin and nitric oxide stop platelets from sticking together
    We don’t want platelets to stick together when there is no damage
  4. Platelet formation regulated by hormone thrombopoietin
57
Q

Hemostasis (Blood clotting)

A
  • Hemostasis: the process by which bleeding is stopped after blood vessel rupture occurs
  • Localized response that progresses very quickly
58
Q

Three steps involved for hemostasis(blood clotting)

A

1) Vascular spasm: rapid constriction of an injured blood vessel. This is Triggered by: A) injured smooth muscle tissue, B) chemicals released by damaged endothelial cells of vessel wall, & C) reflexes from local pain receptors

2) Platelet Plug Formation: platelets stick to each other & to fibers in blood vessel wall to form a plug in a damaged blood vessel

Platelets release the following in response to injury:
1)** ADP:** causes more platelets to stick to site of injury
2) Serotonin, thromboxane A2: increase vascular spasm & platelet aggregation

Platelet plugs are only good for general wear & tear and small injuries (prevent blood loss)
Larger injuries require more severe mechanism to stop bleeding (i.e., coagulation)

  1. Coagulation: formation of a blood clot
59
Q

Three steps involved for hemostasis(blood clotting)

Coagulation process

A

The Process:
A) Several clotting factors (I-XIII) involved to form prothrombin activator (13 of them)
-Clotting factors come from liver

B) Prothrombin activator catalyzes conversion of plasma protein prothrombin into active enzyme thrombin
-Prothrombin is inactive
-Thrombin is an active enzyme (this should be produced when need a blood clot)

C) Thrombin catalyzes transformation of soluble clotting factor fibrinogen into fibrin molecules
-Fibrinogen is soluble
-Fibrin is insoluble in blood

Fibrin molecules link together to form long, insoluble strands that stick together
Factor XIII: enzyme that binds fibrin strands to one another. This contributes to the strength of a blood clot!! It increases strength of strength and decreases likely hood of clot to tear open
Fibrin strands also trap platelets–> forming a blood clot
Anything that tries to pass through (RBCs, etc.) get trapped in “mesh” clot

60
Q

Blood clot retraction

A
  • Definition: the process of pulling damaged edges of blood vessel close together
  • Platelets in blood clot have contractile ability
  • Contraction pulls fibrin strands together & pulls edges of injury closer together (pull edges of damage blood vessels together—> platelets then release platelet-derived growth factor)
  • Platelet-derived growth factor: causes increase in number of fibroblasts and smooth muscle cells in damaged area
    -Forms connective tissue that will eventually form new blood vessel wall where damaged occurred
    -Release collagen fibers that seal up damaged area
61
Q

Fibrinolysis

A
  • Definition: the removal of blood clot after healing is complete
  • Why is this process necessary after healing is complete? Can’t keep blood clots since new blood clots can build up on old blood clots which can block circulation over time

**Plasmin: **enzyme that digests fibrin (when plasmin is released it digests fibrin into amino acid into circulation which is reused for something else)
Typically begins within 2 days of clot formation (very highly dependent on severity of injury)

62
Q

homeostatic imbalances of Blood clotting

Thromboembolic Disorders:

A

Thromboembolic Disorders: formation of undesired/unnecessary blood clots

  1. Thrombus: formation of blood clot in unbroken vessel (remains stuck to vessel wall)
    sits there and builds on itself —> blocking circulation
    Effect: blocks circulation
  2. Embolus: blood clot that starts out as a thrombus and then it breaks free and enters circulation
    Effect:
    -If small, embolus generally not a problem
    -If large, can obstruct smaller blood vessels & block circulation
    -Don’t want to block circulation in the brain
    Example: Ischemic stroke occurs when blood vessels leading up to one side of the Brian is blocked off by embolus. That side of brain no longer gets blood which leads to stroke
63
Q

homeostatic imbalances of Blood clotting

Bleeding disorders:

A

Bleeding disorders: absence of desirable blood clots, leading to excessive bleeding

  1. Thrombocytopenia: low number of platelets in circulation
    -Limited ability of body to form platelet plugs–>even “small breaks” can cause massive hemorrhage
    -Caused by: anything that decreases red bone marrow will usually decrease platelet count
  2. Hemophilia: hereditary bleeding disorders
    -Deficiency or absence of certain clotting factors causes extreme bleeding from small cuts/injuries
    -Symptoms: prolonged bleeding into tissues, painful/disabled joints (limited movement)
64
Q

Homeostatic Imbalances: Bleeding Disorders

Types of Hemophillia

A

1) Hemophilia A: deficiency of clotting factor VIII (8) -most dangerous (more likely to bleed to death from small cuts and injury)
2)Hemophilia B:deficiency of factor IX (9)
3) Hemophilia C: lack of factor XI (11) -most mild (least likely to bleed to death from small cuts and injury)

Treatment:
* Plasma transfusions
* Injections of absent/deficient clotting factor
* People with hemophilia need to be treated frequently

Anatomy Spring semester (10 decks)

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