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Zool 463 > Hematology > Flashcards

Hematology Flashcards

1
Q

Haemostasis

A

Blood blocking

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2
Q

Fluid compartments and composition

—–% of total body weight is water. That is around —- in a 70Kg man

A
  1. 57
  2. 40 litres
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3
Q

Fluid compartments and composition

Blood volume is about —- in women and —– in men

A
  1. 5 litres in women
  2. 5.5 litres in men
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4
Q

Fluid compartments and composition changes with: (2)

A

age and sex

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5
Q

Fluid compartments and composition

Obesity —- the percentage of fluid composition

A

decreases

Increase fat = fluid composition decreases

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6
Q

Fluid compartments and composition

Average intake of water is —- under normal conditions to replace what we use.

A

2.3 lit/day

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7
Q

Fluid compartments and composition

The daily intake and output of water: Skin (2)

composition + amount

A
  • Contains stratum that is not 100% impremeable.
  • 350 ml/day
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8
Q

Fluid compartments and composition

The daily intake and output of water: Lungs (3)

Exercise + Mechanism + amount

A
  • As breathing rate increases you lose more fluid and so prolonged exercise increases fluid loss.
  • When you inhale, air in lungs are saturated with fluid and when you exhale, you lose the fluid
  • Normal = 350 ml/day
    Prolonged heavy exercise = 650 ml/day
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9
Q

Fluid compartments and composition

The daily intake and output of water: sweat (2)

Used to + amount

A
  • Mechanism to cool down
  • Normal = 100 ml/day
    Prolonged heavy exercise = 5000 ml/day
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10
Q

Fluid compartments and composition

The daily intake and output of water: urine (2)

change when + amount

A
  • Change when exercise, more concetrated when the body lose too much
  • Normal = 1400 ml/day
    Prolonged heavy exercise = 500 ml/day
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11
Q

Fluid compartments

There are two main fluid compartments:

A
  1. Intracellular (~28 L)
  2. Extracellular (~ 14 L):
    - Interstitial fluid (11 L)
    - Plasma (~3 L)
    - Small compartments such as CSF, intraocular fluid and fluids of the GI tract etc
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12
Q

Interstitial fluid

Plasma is a —– compartment and interstitital is ——-.

A
  • acellular compartment
  • inbetween the cell
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13
Q

Interstitial fluid (3)

set up + derived from + constituents

A
  • Fluid occupying the space between the cells
  • Derived from filtration from the capillaries
  • Same constituents as plasma except for large proteins which are present at lower concentration
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14
Q

Interstitial fluid

Amount of fluid in the interstitial fluid depends on:

A

Starling forces

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15
Q

Capillaries are lined by —— which has —- in which ——-.

A
  • 1 layer of endothelial cells
  • pores and clefts
  • fatty compounds goes past easily and large protein cannot go past.
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16
Q

Interstitial fluid

Na+ is more in —- because of the ——.

A
  • plasma (outside the cell than inside)
  • Na/K+ pump
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17
Q

Interstitial fluid

Mg+ is —– in the cell as it ——-.

A
  • higher
  • complex with enzymes in cell and contributes in circulation
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18
Q

Interstitial fluid

Free Ca2+ is —– inside intracellular compounds because —–.

A
  • 0
  • theres alot of Ca2+ inside the cell but they are sequestered in the Golgi or ER.
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19
Q

Interstitial fluid

HPO4-, H2PO4- (2)

importance*

A
  • High inside intraceullar because of ATP/ energy formation (*ATP contains three phosphate groups, and during its synthesis and hydrolysis, these phosphate ions are involved in the transfer of energy within cells.
    *) and also acts as a buffer inside the cell.
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20
Q

Interstitial fluid

Inside interstitial fluid, the —- are the same and the —– are different

A
  • ion components (Na+, K+, Cl-, Mg+, Ca2+, HCO3-, HPO4-, H2PO4-)
  • Proteins ( cannot move, too large)
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21
Q

Proteins in interstial fluid in the liver are (2):

what + mechanism/why

A
  • an exception. There are pores large enough for proteins to move through.
  • The liver contains specialized blood vessels called sinusoidal capillaries. Unlike the capillaries in most tissues, these have large fenestrations (pores) and a discontinuous basement membrane.
    These features allow not only small molecules but also larger molecules like proteins to pass freely between the blood and the interstitial fluid.
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22
Q

Solute concentration in intracellular and extracelular compartments provide —- where water moves ——-.

A
  • osmolality
  • from less concentrated to more concentrated
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23
Q

Hyperosmostic

A

drives water

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24
Q

Small solutes can move freely and does not provide ——. Because of pores, whats inside the blood is also inside interstial fluid. Except for proteins which contributes to ——.

A
  • osmotic pressure
  • colloid pressure
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25
Q

Relative permeability of muscle capillary pores and size:

A
  • Permeability index goes down and is inversely related to molecular weight. Larger molecules have more difficulty to go through.
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26
Q

How much and how fast solutes go through capilaries depends on:

A

Molecular weight

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27
Q

Capillaries are a monolayer of endothelial cells and have membrane where —— can go through where cleft and pores allow larger molecules. The pores are —— nM and are —- in liver and —- in the brain.

A
  • fat soluble and small molecules
  • 6-7
  • larger
  • smaller
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28
Q

O2 and H2O in capillary pores

A
  • Goes through no problem
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29
Q

Colloid osmotic pressure/Oncotic pressure (3)

caused by + increases + mechanism

A
  • caused by the presence of proteins
  • increases when protein concentration increases
  • Movement of the water molecule from low osmotic pressure (low protein) to high osmotic pressure (high protein) and more water creates higher volume.
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30
Q

There are 3 major types of proteins in the plasma that contribute to oncotic pressure:

A
  1. Albumin
  2. Globulin
  3. Fibernogen
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31
Q

There are lots of protein/hormone in blood like insulin but they are ——-.

A

not big enough concentration wise to contribute to oncotic pressure.

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32
Q

When you have a kidney disease and lose proteins …..

A
  • you will also lose fluid from plasma to interstial causing swelling and edema.
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33
Q

Albumin (3)

known as + acts as + this helps

A
  • Most abundant plasma proteins; provide colloid osmotic pressure in the plasma
  • Acts as a nonspecific carrier protein. There is no physical nature, binding affinity is low which means it’s dissociation is high. When molecules are bound to carrier (albumin), their half life increase since no enzyme degrades and stays in body longer. Since albumin does not tightly bind its ligands, the molecules it carries can readily dissociate and become bioavailable
  • This nonspecific binding helps transport these molecules through the bloodstream to various tissues or organs for metabolism, excretion, or action.
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34
Q

Globulin (2)

known as + amount

A
  • Proteins with specificity; e.g., specifc carrier proteins, enzymes and immunoglobulins. Interacts with ligand more specifically.
  • Less abundant than albumin
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35
Q

Fibrinogen (2)

what + amount

A
  • Key factor in blood clotting; polymerizes into long fibrin threads during blood coagulation (plug).
  • Least abundant
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36
Q

Colloid osmotic pressure is the osmotic pressure caused by:

A

protein prescence

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37
Q

Colloid osmotic pressure increase when protein concentration —–

A

increases

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38
Q

The 3 major type of protein in the plasma contribution to colloid pressure is ——– to concentration because —-.

A
  • not porprotional
  • molecular nature
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39
Q

Difference between osmotic pressure inside the cell and interstial:

A

Osmotic pressure inside the cell is determined by solutes that contribute and so the movement inside the cell to interstial compartment is determined by different type of factors different then movement from capillary to interstial (colloid).

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40
Q

Fluid movement in and out of the capillary is affected by ——.

A
  • Starling forces
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41
Q

Starling forces:

Outward forces (2):

A
  1. Physical pressure/ Capillary pressure Pc: determined by blood pressure
  2. Interstial fluid colloid osmotic pressure (proteins differ from plasma, etc collagen)
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42
Q

Movement of water outside capillary is a function of:

A

Blood pressure

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43
Q

Increase in colloid pressure —–

A

draws water

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44
Q

Starling forces:

Inward forces (2)

A
  1. Push inward: Interstial fluid pressure doesnt change under normal conditions
  2. Pull inward: Plasma colloid osmotic pressure: proteins inside the blood, determines most of the movements
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45
Q

Talk about the overall starling forces:

A
  • Outward force is 28.3 mmHg
  • Inward force is 28.0 mmHg
    Net outward force towards interstial compartment is 0.3 mmHg.
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46
Q

Draw the starling forces

A
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47
Q

The difference of 0.3 mmHg allows:

A

Slight movement from capillary to interstial.

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48
Q

People with kidney problems have reduce or lose protein in urine which causes —- colloid pressure, —- swelling and more water in the ——.

A
  • low
  • more
  • interstial compartment.
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49
Q

Interstitial compartment cotains (2):

A
  1. Collagen fibers (most abundant)
  2. Proteoglycan filaments
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50
Q

Collagen fibers (3)

Pressure + flunctation + amount

A
  • increase colloid pressure in intersitial comparemnt
  • Do not flunctauate from day to day, stays constant (unlike albunium) and any change will be age related.
  • Most abundant in interstitial
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51
Q

Proteoglycan filaments (3)

component (2) + importance

A
  • 98% hyaluronic acid ( a muccopolysccharide/carbohydrate)
  • 2% protein
  • ~99% of interstitial fluid is entrapped among the proteoglycan filaments resulting in the characteristics of a gel (tissue gel). Only 1 % of water is present as free flowing fluid (~1%)
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52
Q

Hyaluronic acid is used to:

A

do face injections

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53
Q

How is waste from cells like CO2 taken care off?

A
  • 10% in lymphatic system
  • 90% back to circulation (venous)
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54
Q

Intersitial compartment:

Movement of solutes in the Intersitial compartment is by:

A
  • molecular diffusion through the gel (95-99% as rapid as in fluid) Not tampered by gel
55
Q

Conditions that increase fluid in the intersitial compartment results in —– (an increase in the small pocket of free fluid). This may results from ——

A
  • edema
  • changes in osmotic colloid pressure
56
Q

In kidney failure explain what leads to Edema and the process:

A
  1. Excretion of protein = reduce colloid pressure change in circulating protein
  2. More fluid in interstitial increase free fluid as there’s a finite capacity to form the gel.
  3. Swelling (Edema)

Two factors leading to Edema:
- Changes in colloid pressure
- Distruption in starling forces

57
Q

Prescence of proteoglycan, gel formation and collagen support ensures (3):

A
  1. Uniform distribution of fluid compartments within the body regardless of body position and prevention of fluid accumulation due to gravity. Gel doesnt flow down with gravity so lower part has no swelling
  2. Maintenance of optimal intracellular distance allowing uniform diffusion of dissolved gases and solutes (required for solute movement)
  3. Mechanical support- Giving shape to body parts (push your nose -> doesnt change shape)
58
Q

Explain the capillaries to lymph flow process:

A
  1. blood from venus system goes into capillaries
  2. Movement of O2, nutrients into interstitial component as theres a net flow of 0.3mmHg.
  3. Cell in tissue use these for metabolism
  4. Produce waste product, CO2
  5. 90% of waste goes back to venous system (circulation), 10% goes into lymphatic system
59
Q

Fluid movement from capilliaries into lymph due to —–

A

-0.3mmHg pressure difference

60
Q

Lymphatic also has —– that cause some contractice movement. There is also —- in which macromolecules even cells can go through but not backtrack.

A
  • myofilament
  • one-way valves
61
Q

Lymph system (3)

What it is + process + resistance

A
  • An accessory route for the transport of fluid and macromolecules from interstitial space to veins
  • Lymph is filtered through lymph nodes in neck region (containing phagocytic cells), which act as filteres to remove foreign blood contaminants before drainage into veins (circulation)
  • No resistance as small amount of pressure allows circulation to take place.
62
Q

Lymph flow is a function/—– of —-

A

porprotional
interstilial fluid pressure

63
Q

When you block lymphatic system you will have:

64
Q

Lymph flow

Elephantiasis (2)

Caused by + what happens

A
  • Caused by thread-like filarial worms transmitted into the blood by misquitos.
  • The worms and inflammatory reactions to the parasite block lymphatic flow in different areas causing lymphedema. Then the increase pressure stops any movement of fluid, blocks starling forces and fluid stops flowing into the tissue so you have no O2 or nutrients (necrosis)
65
Q

Other small fluid compartments (5):

A
  • CSF: cushion brain
  • Intraocular fluid: maintains succificient pressure in the eyeball to keep it distended
  • Fluid compartment of the GI tract (Potential space ~ 15 ml which allows absorption of nutrients)
  • Fluid compartment of the lung: (Pleural cavity; mucoid fluid ~10ml provide lubrication for easy slippage of the moving lung
  • Fluid compartment of pericardial cavity, peritoneal cavity, joint space, bone and cartilage
66
Q

Pluripotential haemopoietic stem cells (PHSC) (3)

production site + what happens with it + changes

A
  • produced in bone marrow
  • Go through self-proliferation
  • Site of production and plorliferation change with age
67
Q

Explain the PHSC differentiation process (4):

A
  1. You start off with uncomitted stem cells that proliferate and produce more of the same.
  2. They might migrate to lymphatic
  3. Differentiation factors such as cytokine which acts on undifferntiated cells and change gene expression pattern marking it to be a certain kind.
  4. Myeloid stem cells in the bone marrow become RBC, platelets, neutropil + monocyte + basophil + Eosinophil (granulocyte) and lymphoid stem cells become lymphocytes (immune)
68
Q

Take home:

Different stem cells are large in ——- or —- system and differentiate
Ones in —— are differentiatble to —– which has —– types.

A
  • bone marrow
  • lymphatic
  • lymphatic system
  • lymphocyte
  • two types
69
Q

Draw the diagram of PHSC differentiation

70
Q

Production of blood cells: Haemopoiesis

Cytokines

A

Control proliferation and differentiation of blood cells

71
Q

Once differntiation starts following ———- the cells are called —– and are destined to become a specific group of blood cells. There is ——.

A
  • stimulation by differentiation factors
  • commited progenitor cells
  • no going back
72
Q

Interleukins and stem cell factor (3)

What group + what they do + molecular composit.

A
  • Different group of cytokines
  • Increase production of all haemopoietic stem cells
  • Peptide and protein that act through membrane receptor (cytokine receptor) and make more haemop. cell
73
Q

Examples of specific differentiation factors (3)

A
  1. Erythropoietin: Stimulates myeloid stem cells to differetiate to erythrocyte (RBS)
  2. Thrombopoietin: Stimulate differentiation to megakaryocyctes (cells that break off to produce platelets)
  3. Granulocytes-Monocytes Colony stimulating factors stimulate differentiation to Granulocytes and Monocytes.
74
Q

Polynuclear cells (2)

What + includes

A

Cells with different shaped nucleus have granular appearance also know as GRANULOCYTES
- Neutrophils, eosinophils, Basophils

75
Q

Draw the Vertical diagram of blood cells categorization:

76
Q

Monocytes form

A

macrophage

77
Q

What cells are part of the WBC category? (7)

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
  4. Monocytes
  5. Plasma cells and B cells
  6. T Lymphocytes
  7. NK cells
78
Q

Red Blood cells (4)

nucleus + shape + diameter/thickness + can….

A
  • Mature red blood cells have no nucleus (anucleated)
  • Has deformable membrane biconcave disks
  • ~8u in diameter and 1-2u in thickness
  • RBC can change shape and pass through small capillaries
79
Q

Red Blood cells (4)

Amount + blood volume + hematocrit + anemia

A
  • Most numerous in blood
  • Constitute ~48% of blood volume in male and ~42% in female Hormonal difference
  • Hematocrit- a measure of the porprotion of volume that is occupied by red blood cells: determined by centrifugation (see colour seperation to measure percentage
  • In severe anemia hematocrete may decrease to ~10% - may result in death
80
Q

Red Blood cells main function (3):

A
  1. Transport of hemoglobin which is the most important oxygen carrier molecule. Can reversibly bind to O2 and depending on O2 concetration, O2can dissociate from hemoglobin when O2 levels are low in peripheral blood.
  2. Hemoglobin also acts as an important acid-base buffer for the blood (Proton donor or acceptor)
  3. RBC contains carbonic anhydrase which catalyzes production of bicarbonate
81
Q

Carbaminohemoglobin

A

Small amounts of CO2 can bind to hemoglobin and produce carbaminohemoglobin. Does not bind to the same side as O2 so no competition. Binding of carbon dioxide to hemoglobin is reversible. Therefore, when it reaches the lungs, the carbon dioxide can freely dissociate from the hemoglobin and be expelled from the body.

82
Q

Production of erythocyte throughout the years (2):

where + aging

A
  • After birth, RBC are produced only by the bone marrow from PHSC (number decline with age)
  • As you age, the bone marrow in long bone have build up of fat (tibia, femur) that prevent haemopoetic stem cell to proliferate.
83
Q

Commited cells that become erythrocytes are called:

A

Colony forming unit-erythrocytes (CFU-E)

84
Q

Explain the complete path of RBC production (7):

A
  1. EPO produced in kidney and liver stimulates myeloid stem cells (uncomitted) to erythrocytes (commited)
  2. Proerythoblast: Nucleus proliferate like crazy
  3. Basophil erythroblast: Can stain with basic dye.
  4. Polychromatophil Erythoblast: Mitotic (need protein synthesis for globin), Hb start to appear the different colour can stain + start to be red as produce Hb, divide like crazy
  5. Orthochromatic erythroblast: No mitosis, Hb level increase
  6. Reticulocyte: Nucleus disappear; move to blood from bone marrow. No cell division/mitosis (mRNA leftover make protein)
  7. Erythrocytes: organelles disappear, have all the enzymes. There is only a 3 month lifespan because no nucleus mean runs out of protein. Membrane integrity will decrease and phospholipid can change but protein is not there. Before rupture, macrophage eats it.
85
Q

Hemoglobin (5)

what/synthesized where + adult + fetal + O2 + subunits

A
  • Iron containing molecule synthesized in erythroblasts
  • Hb A (2 alpha + 2 beta) is the most common form in the adult human
  • In fetal Hb (2 alpha + 2 gamma) has greater affinity for O2 and can carry 20-30% more O2 (it’s concentration is also ~50%. greater than adult Hb). This is beause in adult, hemoglobin easily binds to O2 to peripheral blood and is reversible to release, fetal Hb competes with maternal peripheral blood to extract O2.
  • Each iron atom can bind with one O2 therefore, each Hb molecule (containing 4 iron atoms) can carry four O2 molecules.
  • Hemoglobin has 4 subunits and 4 heme groups each containing one Fe2+ molecule. Each Fe2+ binds to one O2 molecule, therefore, each Hb molecule carry four O2 molecules.
86
Q

CO role in hemoglobin

A

CO can bind to heme and is not reversible. Cannoy carry O2 anymore.

87
Q

The Fe2+ - O2 bond is:

A

Easily reversible

Or else cant come off in peripheral blood

88
Q

Hemoglobin synthesis pathway (6)

A
  1. Succinyl-CoA (product of metabolism
  2. Pyrrole
  3. 4 pyrroles come together to make protoporphyrin (poor solubillity)
  4. Protoporphyrin and iron come together to make heme (4 protoporphyrin and iron)
  5. Heme and globin (peptide: a,b,y or delta) to make Hb subunit (a, b, y or delta) 4 type of hemoglobin based on globin
  6. Functional Hb consists of 4 subunits (2 a + 2 B to make hemoglobin A) Require 4 hemoglobin to come together
89
Q

Molecular basis of sickle cell anemia (2)

what occurs + results

A
  • Single point mutation: glutamic acid (hydrophilic) is replaced by valine (hydrophobic) at position 6
  • Changed codon (1 amino acid changes) and sickle cell have different property. They will lose the ability to move through small capillaries and will crystalize when there is no O2 (hypoxia) which occurs in the peripheral. They can cause rupture at tight spaces.
90
Q

When O2 binds to hemoglobin:

A

When O₂ binds to hemoglobin, it induces a conformational change in the hemoglobin molecule. This change reduces hemoglobin’s affinity for CO₂, facilitating the release of CO₂ in the lungs for exhalation.

Footnote: This process is a part of the Haldane effect, where oxygenation of blood in the lungs reduces hemoglobin’s ability to carry carbon dioxide and hydrogen ions, promoting CO₂ release.

91
Q

—– is the RBC differentiation factor, a glycoprotein produced mainly in the —– (80-90%). When it comes across myeloid stem cells it converts to proerrythrocytes.

A
  • Erythropoietin
  • kidney
92
Q

Hypoxia and RBC:

A

Hypoxia stimulates the production of erythripoietin which in turn stimulates the production of proerythroblasts and RBC (~5 days)

93
Q

Why do athletes come to calgary to train?

A

High amplitudes cause hypoxia. In calgary, we have low O2 tension then ocean levels. Athletes come here to train (hypoxic conditions) so hemoglobin levels goes up and have an advantage.

94
Q

Low O2 levels can be caused by (5)

A
  • Low blood volume (hemmorrage)
  • Anemia
  • Low hemoglobin (iron deficiency)
  • Impaired blood flow to lung
  • Pulmonary disease that lead to hypoxia
95
Q

Factors affecting RBC production:

Vitamin B12 (3)

what happens + phases caused by

A
  • Lack of vitamin B12 or Folic acid (B9) results in reduced DNA synthesis and failure of nuclear maturation impaires the formation of RBCs
  • Cells cannot progress from the G2 growth phase to mitosis and enlarge causing megaloblastic anemia. (synthesis goes on but dont divide, interupted at interphase)
  • Usually caused by impaired absorption of vitamine B12 due to GI problems
96
Q

Factors affecting RBC production:

Iron metabolism (3):

Total body content + storage

A
  • ~ total body content ~4g (in form heme in the body)
  • 65% in the form of hemoglobin (myoglobin also contain some iron)
  • 15-30% stored as bound to Ferritin (specific binding protein for iron produced) mainly in the liver. Stores it day to day when you take more or less iron, it stabilizes it.
97
Q

Factors affecting RBC production:

Iron metabolism (3):

process of how iron goes into RBC + abnormalities

A
  • Once iron is released from ferritin, it binds to a plasma protein known as transferrin (b-gobulin) which change conformation and form affinity for receptor on surface of erythroblast in the bone marrow.
  • Gets endocytosed (iron) and delivered to mitochondria to make heme molecules.
  • Abnormalities in transferrin results in anemia.
98
Q

“The saturability of transferrin in the blood limits the absorption of iron from intestine (feedback mechanism)”
Explain what this mean:

A
  • There is finitie amount of transferrin in the blood so it is saturable. This saturability of transferrin determines how much iron used and transport of iron in GI to mucosa cell. Transferrin enters bile and gets discharged in GI tract to bind to iron. Transferrin binds to dietary iron to transport to mucosa and the blood.
99
Q

Movement of iron into erythroblast is not —-. It has to bind to —– and the complex binds to erythroblast receptor and gets —– to make the synthesis of —–

A
  • passive
  • transferrin
  • endocytosed/internalized
  • hemoglobin
100
Q

Destruction of RBC (4)

lifetime + what happens + nucleus + overtime metabolic activies

A
  • Average lifetime of RBC is ~120 days
  • After that, membrane gets leaky (metabolites released) and imune system is notified so macrophages can gobbled up RBC. Small portion of RBC do go through hemolysis.
  • Although RBC does not have nucleus and other organelle, it has cellular enzyme capable of limited metabolism to form ATP and other compounds.
  • Metabolic capability progressively deteriorates with time resulting in membrane weakening and rupture of RBC particularly in the tight spots in the spleen.
101
Q

Destruction of RBC (3)

The main mechanism + iron + porphyrin

A
  • Damaged RBC is mainly phagacytosed by macrophages as secretatory products are released from RBC
  • The released iron binds to transferrin for synthesis of new hemoglobin ad well as binding with ferritin for storage
  • The porphyrin portion of the hemoglobin which has poor solubility is converted to bilirubin (hydrophillic) which is released into the blood and the bile.
102
Q

In urine, high level of bilirubin means:

A

Abnormal breakdown of RBC

103
Q

RBC that are not taken by macrophage after burts cause:

A

inflammation

104
Q

Platelets (3)

What + replication + contains

A
  • Small oval disc of 2-4u in diameter derived in the bone marrow from large megakaryocytes (150,000 - 300,000/ul; t1/2 = 8-12 days)
  • They cannot replicate or divide
  • Contains all component except nucleus
105
Q

Platlets do not have nucleus but contains (5):

A
  1. Surface glycoprotein receptors that recogizes collagen and damaged endothelial tissue. Normally does not come into contact with collagen because platelets are in blood unless rupture and contact IST collagen.
  2. Actin, myosin and thrombosthenin (contractile filaments) that can cause the platelets to contact and change shape
  3. Residuals of both ER and golgi apparatus therefore can make some enzymes and store Ca2+ (surface receptor can produce cpmpound that release Ca2+ stored which is important for enzyme activation)
  4. Mitochondria and enzymes to produce ATP and ADP (important because lots of activities going on and release of compound that are energy dependent)
  5. Platelet surface proteins activates enzyme system to produce eicosanoids (thromnoxane A2).
106
Q

Platelet cytoplasm also contains —- and a number of —– used for injuiry damaged tissue growth.

A
  • fibrin-stabilizing factor
  • growth factors
107
Q

Haemostasis and blood coagulation

Vascular constriction (reflex) results from a cut or rupture of a blood vessel due to (2):

A
  • Local myogenic spasm (smooth muscles): partially stimulated by thromboxane A2 released by platelet cells (activated by collagen in tissue matrix)
  • Nervous reflex: initiated by activation of pain receptors (other compounds produced that activate pain pathway)
108
Q

Haemostasis and blood coagulation

Platelet activation (3):

activation + release + precursor

A
  • Upon contact with damaged vascular endothelium, the surface recptors are activated resulting in platelet cell activation.
  • Once activated platelet release ADP and thromboxane A2 which activate other platelet cells
  • ADP is precursor of ATP and ATP acts as a messenger molecule
109
Q

Escosanoids are derived from:

A

Phospholipids and arachidonic acid

110
Q

Patients with thrombosis treatment:

A

You put patients on low dose of aspirin which is an inhibitor of COX- II. This limit/reduce thromboxane A2 which reduce thrombosis.

111
Q

Explain the full steps of platelet activation at a site of injuiry (5):

A
  1. Platelte contact with collagen due to trauma which activates membrane receptors
  2. Activates production of thromoxane A2 and ADP (secretes ADP in the vessicles)
  3. ADP causes swelling and the production of protruding processes that bind to other platelet cells. They stick to one another.
  4. Thromboxane A2 activates other platelet cells and formation of the platelet plug.
  5. The activated platelets also produce fibrin-stabilizing factor which is necesary for forming fibrin meshwork and clotting. Fibrin thread binds to sticky platelets and endothelian to reinforce plug.
112
Q

Blood coagulation

Blood vessel trauma results in the activation of —- and —– factors leading to the activation of —— and blood coagulation.

A
  • extrinsic
  • intrinsic
  • thrombin
113
Q

Blood coagulation

Thrombin (2)

Originates + what it does

A
  • Prothrombin to thrombin via proteolysis
  • Converts fibrinogen which is globular and in circulation to fibrin threads. Thrombin breaks fibrinogen down to a monomer and reconfigure/realign from globular to a linear fibrous protein.
114
Q

What role does ca2+ play in blood coagulation?

A
  • Platelet cells reinforce cross linking between fibrin threads and release Ca2+ which is required for the process of clot formation. Removing Ca2+ you will remove the coagulation potential.
115
Q

Thrombin (enzyme) is a proteolytic product of —- produced in the —- due to the action of ——.

A
  • prothrombin
  • liver
  • vitamin K
116
Q

Factors that initiate blood coagulation

Factor XII (3)

aka + what it does + initiates

A
  • Hagemen Factor
  • Initiates intrinsic pathway following blood trauma. Contact of this factor with platelet and collagen or wettable surface results in configuration change and activation which in turn activates other factors -> clotting
  • Initiates activation of factor X
117
Q

Factors that initiate blood coagulation

Factor III (3)

aka + initiates + present in

A
  • Tissue thromboplastin
  • Initiates extrinsic pathway (lipoprotein and phospholipid present in endothelian cells). Released from tissue following trauma. Damaged endothelian tissue release tissue thrombin.
  • Present in endothelian cells
118
Q

Hagemen factor contact with platelet, collagen or wettable surface/tissue matrix:

A

Results in cleavage of HF and becomes activated into Factor XIIa

119
Q

What steps in blood coagulation requires Ca2+ (5)?

A
  • 11 to 9
  • 9- 10
  • TTPlastin to 10
  • Prothrombin to thrombin
  • Fibrinogen monomer to fibrin fibres
120
Q

Both intrinsic and extrinsic leads to:

A

Activation of factor X

121
Q

—- mainly activates intrinsic and —- activates extrinsic

A
  • Sharp cut
  • Hit hammer with finger
122
Q

Synomons

Fibrinogen

123
Q

Synomons

Prothrombin

124
Q

Synomons

Tissue factor

A

Factor III; tissue thromboplastin

125
Q

Synomons

Calcium

126
Q

Synomons

Factor X

A

Stuart factor

127
Q

Synomons

Factor XI

A

Plasma thromboplastin antecedent (PTA); antihemophillic factor C

128
Q

Abscence of Factor VII or mutation (antihemophillic) (3):

causes + affects + what it does

A
  • Hemophilia
  • X-linked, recessive trait in female; ie. most females are carrier, only males are affected
  • Slows down blood clotting
129
Q

Factor V

A
  • Proaccelerin
  • Only present in local injuiry site, priduced and accelerate
130
Q

Eicosanoids (thromboxane A2) are derived from

A

phospholipids and then arachidonic acid

131
Q

prostenoids are formed in the COX-II pathway and include:

A

thromboxane, prostaglandins, prostacyclins

132
Q

All of the eicosanoids produced by arachidonic acid (in COX-II and lipoxygease pathways):

A

COX-II: thromboxane, prostaglandins, prostacyclins
lipoxygease: leukotriene

133
Q

What do platelet cells do to fibrin threads for clot formation

A

reinforce cross-linking between fibrin threads and release calcium (required for clot formation)

134
Q

what 2 things increases production of all haemopoietic stem cells?

A

interleukins and stem cell factors (these are NOT differentiation factors)

Zool 463 (8 decks)

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