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PHYG 209 > Blood > Flashcards

Blood Flashcards

1
Q

What are the main blood functions?

A
  1. Transport:
    - Nutritive
    - Respiratory
    - Excretory
    - Hormone
    Temperature regulation
  2. Acid-Base balance:
    - Normal pH range
  3. Protective:
    - some blood cells and some proteins
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2
Q

What is the composition of blood (%)?

A

55% Plasma (liquid part)
45% Erythrocytes/RBC
Buffer layer (WBC and platelets)

*Plasma counts ECF (plasma) and ICF (inside blood cells)

around 7% of body mass

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3
Q

What are the terms for:
Normal blood volume
Lower blood volume
Higher blood volume

A

Normal = Normovolemia
Lower = Hypovolemia
Higher = Hypervolemia

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4
Q

What is the Hematocrit?

A

Clinical index
Percentage of blood volume occupied by RBC

Measured with column –>
height of RBC/hiegh of whole *100%

Normal Ht = 45%

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5
Q

Voir p.12 for example

A
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6
Q

What is the global composition of plasma?

What is the main difference between composition of Plasma and ISF

A
  1. more than 90% = water
  2. ions
  3. Nutrients (Glucose, amino acids, lipids) wastes (urea, lactic acid, etc.)
  4. Resp. Gases: O2, CO2 (in small concentration because rapid exchanges with other parts of the body)
  5. proteins (colloid) = 7g%
    - Albumins 60%
    - Globulins 35%
    - Fibrinogen 5%

*Main difference = presence of protein in plasma

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7
Q

What are the different ways to separate Plasma proteins?

A
  1. Differential Precipitation by Salts
  2. Sedimentation in Ultracentrifuge
  3. Electrophoretic Mobility (most clinically used)
  4. Immunological Characteristics
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8
Q

How does electrophoresis work?

A

1 of the ways to separate plasma proteins

Fractionation method based on mvt of charged particles along voltage gradient (migrate from anod- to catod+)

Rate of migration influenced by number and distribution of charges + by MW of each protein

Make stains –> area under peak in scan = concentration in blood

When concentration changes –> disease

Voir p.17-18

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9
Q

Where do the plasma proteins come from?

A

Liver:
Albumin, Fibrinogen, Globulins (a1, a2, b)

Lymphoid Tissue:
y Globulins (bc they are antibodies)

*When liver diseased –> plasma protein level decrease

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10
Q

What is the shape, the MW range, the concentration and COP of the different plasma proteins?

A

Albumin:
small oval, 69Kd, 4g%, 20 mm Hg

Globulins:
heterogenous, 90-800Kd, 2.7g%, 5 mm Hg

Fibrogen:
long fiber(oval), 350Kd, 0.3g%, < 1mm Hg

*total of 7g% (= 7g/dl = 70g/L?)

*total odf 25 mm Hg

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11
Q

What in the role of plasma proteins?

A

Determine distribution of fluid between plasma and ISF compartment by controlling transcapillaries dynamics

(ISF doesn’t have proteins)

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12
Q

What is the difference between the cell membrane and the cappillary walls?

A

Cell membrane = impermeable to ions

Capillary walls =
freely permeable to H2O and ions

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13
Q

What is the approximated concentration of ions in ECF?

A

0.9g% solution of NaCl = 300 Osm (6.7 atm or 5100 mm Hg)

*ECF = ISF + Plasma
*Ions = diffusible

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14
Q

How is osmolarity calculated?

A

1 M of solution = 1mol/L = x g/L –> Molarity
concentration in g/L / 1M =

Osmolarity = when dissolved (ions separated)
if seperated into 3 ions, Osm = 3xMolarity
*Practice calculating

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15
Q

What is required to have a net flow of water between compartments?

A

Has to be a difference in osmotic pressure (between both sides of capillary walls)

*Only Non-diffusible solutes contribute to the effective o.p. (can’t go through the capillary wall bc else, become =lly distributed)
Plasma proteins = non-diffusible proteins (only in plasma)

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16
Q

What is the main difference between ISF and Plasma?

How does the net flow change?

A

The presence of plasma protein –> non-diffusible

They then create osmotic effect –> Colloid Osmotic/Oncotic Pressure (C.O.P.) of Plasma = 25 mm Hg

If COP changes, net flow changes:
If COP ↑, water flow into Plasma (to ↓ concentration)
If COP ↓, water flow into ISF (to ↑ plasma concentration that just ↓)

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17
Q

Which are the 2 major forms of fluid tranport across the capillary wall?

A
  1. The COP fo plasma determines amount water move into/out of capillaries
  2. Bulk Flow: flow of molecules subjected to pressure difference

magnitude of Bulk Flow directly proportional to hydrostatic pressure difference

Filtration across porous membrane (like sieve)

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18
Q

What are the 2 important transport mechanism across capillaries?

How are these forces refered to?

A

STARLING FORCES
1. Filtration:
push out fluid from inside capillaries

  1. Osmotic Flow: (due tu plasma prots)
    pull in/retain fluid inside capillaries
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19
Q

What is th capillary bed?

A

site where exchanges take place between plasma and ISF
Filtration in 1st half and absorption in 2nd half

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20
Q

How do nutrients, wastes, O2 and CO2 move in and out of the capillaries?

A

by simple diffusion

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21
Q

What do starling forces determine?

How much is filtered out and reabsorbed directly?

A

Distribution of EFC volume between Plasma and ISF

90% bc 10% is drained by lymphatic vessels

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22
Q

How are the wall of lymphatic vessels?

A

Single layer of endothelial cells

Highly permeable to all ISF constituents (including proteins which may have leaked out of plasma)

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23
Q

What is considered part of the lymphatic system?

A

Lymph nodes
Thymus
Spleen
Bone marrow

Converges and drained into larg veins in the chest

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24
Q

What impacts the colloid osmotic pressure?

A

The NUMBER of osmotically active molecules/unit volume (not size or charge)

Each protein fraction = osmotic pressure:

Directly related to concentration in plasma

Inversly related to molecular weight

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25
Q

Which are the factors that influence the trasncapillaries dynamics?

A
  1. Hydrostatic pressure
  2. C.O.P
  3. Capillary permeability (some may become more permeable and allow some proteins to go in ISF)
  4. Lymphatic drainage
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26
Q

What is EDEMA?

What are the conditions leading to it?

A

accumulation of excess fluid in interstitial space

  1. ↑ Hydrostatic pressure
  2. ↓ Plasma proteins (COP)
  3. ↑Capillary permeability
  4. X obstruction of lymphatic drainage
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27
Q

What can cause a decreased COP?

Voir slides 63-65 pour autres choses

A
  1. Failure to synthesis plasma proteins (ex: liver disease)
  2. Sever malnutrition (no amino acids)
    1st to 2nd baby syndrom –> Kwashiorkor
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28
Q

What is the role of plasma proteins?

A
  1. Major role in determining the distribution of fluid between the plasma and ISF by controlling transcapillaries dynamics
  2. Contribute to viscosity of plasma (maintenance of blood pressure)
  3. Contribute to buffering power of plasma (normal pH range aroung 7.4)
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29
Q

What is the function of:
fibrinogen and some globulins?

y-globulins (immunoglobulins)?

Albumins and some globulins?

A

fibrinogen and some globulins:
clotting

y-globulins (immunoglobulins): specific resistance to infection

Albumins and some globulins:
carriers for lipids, minerals, hormones

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30
Q

What is the word that refers to the production of blood cell?

to the production of RBC?

to the production of platelets?

to the production of WBC?

A

all blood cells: Hematopoiesis

RBC: Erythropoiesis

platelets: Thrombopoiesis

WBC: Leukopoiesis

31
Q

What is the process of Hematopoiesis?

Which are the sites of Hematopoiesis?

A

pluripotent hematopoietic stem cell are differentiated into Lymphoid stem cells or Myeloid stem cells under influence of HGFs
Myeloid then in redifferentiated into erythrocytes and many other Leukocytes

  1. Pluripotential Stem Cell do self-replication (inducer) –> division
  2. They are diferentiated by stimulant? into committed Stem Cells (Leukocytes, Platelets/Thrombocytes and Erythrocytes)

Yolk sac (1 month and 9 months) and Liver and Spleen (3-7 months) for prenatal
Postnatal –> Bone marrow (axial skeleton)

32
Q

What are Cytokines?

What is the specific/important one in our blood?

A

Proteins or peptides which are released by one cell and affect the growth, development and activity of another cell

Hematopoietic Growth Factors (HGFs) influence proliferation and differentiation of blood cell precursors

33
Q

What is the fonction of Erythrocytes?

A

Facilitate transport of respiratory gases between lungs and cells

34
Q

What shape do Erythrocytes have and what the characterstics of it?

How many are there in the body?

A

Biconcave disk

Shape due to presence of spectrin (fibrous protein)

Adantages of that shape:
1. Maximal surface area and minimal diffusion distance for volume –> more efficient O2 and CO2 diffusion

  1. High flexibility (squeeze through narrow capillaries)

Male –> 5.1-5.5x 10^6 / microL
Female –> 4.5-4.8 x 10^6/ microL

*Rate of production = rate of destruction = environ 2 x 10^6/sec

*In RBC no ribosome nor nucleus, just solutes dissolved in water (33% Hb)

35
Q

What 2 enzyme systems do RBC have?

A

Glycolytic enzymes –> generate Energy

Carbonic Anhydrase –> CO2 transport

36
Q

How does Hb (hemoglobin) interact with O2?

*Voir p.86-87 schema

A

Each molecule of Hb can bind with max 4 O2 molecules

When combined with O2 = OXYHb
When released from Hb = DeoxyHb

(needs feritin to bind??)

37
Q

What are Hb functions?

A
  1. Transport O2
  2. Transport CO2
  3. Act as a buffer
38
Q

Where is hemoglobin in the blood? What are the advantages of that?

A

Inside the cell (RBC) instead of dissolved in plasma
Advantages:
1. reduce? Plasma viscosity
2. re Plasma COP
3. re Loss via Kidney

  • Solubility of O2 in plasma = very low: 0.3 mL O2/100mL plasma

but in blood, bc Hb carrying capacity = 20mL O2/ 100mL blood

39
Q

Which are the factors affectiong the ability of Hb to bind and release O2?

A
  1. Temperature
  2. Ionic Composition
  3. pH
  4. pCO2
  5. Intracellular enzyme concentration
40
Q

How does the RBC change to be differentiated from Stem cell (18μm) to Erythrocyte (7μm)?

A
  1. Decease in size
  2. Loss of nucleus
  3. Accumulation of Hb
41
Q

What are reticulocytes?

A

Reticulocytes = immature RBC

Reticulocyte count reflects the amount of effective erythropoiesis in bone marrow
Normal count < 1%

42
Q

What factors determine the # of RBC?

A
  1. O2 requirements
  2. O2 availability
43
Q

What happens when we go up in altitude?

A

pO2 (mm Hg) decreases –> less availability

RBC increase –> be able to carry more

44
Q

What is Erythropoietin?

How is its production regulated?

A

A glycoprotein hormone/cytokine produced largely by the kidney

Hypoxia (not enough O2) stimulates its release –> may come from ↓ # RBC, ↓ availability of O2, ↑ tissue demand for O2

*Erythrpoiesis regulated by release of not of Erythropoietin in kidney depending on its O2 supply –> goes in plasma to bone marrow where RBC produced
–> maintain of HOMEOSTASIS

45
Q

What happens in case of severe accidental hemorrhage?

A
  1. ↓ Hb available for O2 transport
  2. ↓ supply of O2 to kidneys
  3. ↑ production and release of erythropoietin
  4. ↑ produciton of erythrocyte precursors in bone marrow
  5. ↑ discharge of young erythrocytes in blood
  6. ↑ More Hb for O2 transport
46
Q

On which cell does erythropoietin act?

A

EPO stimulates proliferation of Committed stem cells (already committed to becoming RBC), does not act of pluripotent stem cells

Accelerated maturation from committed stem cells ot reticulocytes (not from reticulocytes to mature RBC)

47
Q

What effects do hormones have on erythropoietin?

A

testosterone ↑ release of EPO
testosterons ↑ sensitivity of RBC precursors to EPO

Estrogen ha opposite effects

*This is why men have more RBC than women

48
Q

What is the lifespan of RBC?

How are they disposed of?

A

120 days (nothing prolonges it!!)

Old RBC are recognized and removed by phagocytosis by macrophages in the spleen (some in the liver)
Some also hemolyze in the blood stream

When phagocytosed, old RBC are digested (cell membrane) by enzymes in cytoplasme of macrophage and contente released in its cytoplasme

49
Q

What happens when the content of RBC is released after it has been phagocytosed by a macrophage?
Voir p.119

A

Hb is divide back into heme and globin

Globin –> amino acid pool (reutilized for protein synthesis)

Heme –> oxydized into another pigment Biliverdin (green) –> Bilirubin (yellow) –> into liver which converts it into bile (with other things) –> intestianl tract (color fecal matter)

Iron picked up by Transferrin (albumin) bc toxic and reused as non-toxic way –> if no immediate need, stored in Liver, Spleen, Gut

50
Q

What quantity of bilirubin must be present in plasma?

What effect does a high quantity will have? How does it happen?

A

1mg/dL in plasma –> gives the yellow cooler

If concentration is to high –> jaundice (Icterus)
Causes:
1. Because excessive Hemolysis
2. Hepatic Damage (liver damage)
3. Bile duct obstruction (carries bile from Liver to intestinal tract)

Neonatal jaundice –> excess of blood cells –> to much bilirubin –> can penetrate into brain if not treated

51
Q

What are the clinical indices for RBC?

A
  1. # of RBC
  2. Amount of Hb
  3. Hematocrit
52
Q

Does a low of high hematocrit always mean there is anemia or polycythemia?

A

No, because plasma fluctuates with the amount of water in the body

High hematocrit = polycemia OR dehydratation

Low hematocrit = Anemia OR fluid retention

53
Q

What is polycythemia?

what are the 2 types?

WHat is the problem with polycythemia?

A

When the hematocrit is to high
> 18g% Hb or > 6x10^6 RBC/µL

Normal = 16g% or %-5.5x10^6 RBC/µL

Relative –> due to ↓ plasma volume

Absolute :
1. Physiological
2. Pathological

Problem: ↑ blood vicosity –> sluggish blood flow –> blood clots

54
Q

What can cause physiological (absolute) polycythemia ?

A

*Too high hematocrit
secondary to ↑ O2 needs, ↓O2 availability

  • high altitude
  • ↑ physical activity
  • chronic lung disease (ex: emphysema)
  • heavy smoking (high CO in blood)
55
Q

What can cause pathological (absolute) polycythemia ?

A

*Too high hematocrit

  • Tumors of cells producing Erythropoietin
  • Unregulated Production by Bone Marrow

Polycythemia vera - 7-8x10^6 RBC/uL or Ht 70%

56
Q

What is anemia ?

A

↓ in the oxygen-carrying capacity of blood
1. RBC count ↓ (< 4x10^6/uL for male, < 3.2x10^6/uL for female)
2. Hb content ↓ (<11g% for male, < 9g% for female)

57
Q

What are the different types/classifications of anemia?

A

Morphologic:
- Microcytic (<80 u cube) –> smaller
- Normcytic (80-94)
- Macrocytic (> 94) –> larger

  • Normochromic (33%) –> darker bc 1/3 volume is Hb
  • Hypochromic (< 33%) –> less Hb
58
Q

What are the Etiologic Classes of Anemia?

A
  1. Diminished Production
  2. Ineffective Maturation
  3. Increased Destruction
59
Q

What are the 3 types of diminished production (Etiologic Classification of Anemia)?

A

3 causes:
1. Abnormal site:
Aplastic (hypoplastic) Anemia
Problem with functionning of stem cells in bone marrow
Etiology(causes): unknown, exposure to radiation, chemicals or drugs
Classification: Normocytic, Normochromic

  1. Abnormal stimulus:
    Stimulation failure
    Etiology: renal disease
    Classification: Normocytic, Normochromic
  2. Inadequate raw materials:
    Iron deficiency Anemia (most common)
    Etiology: - ↑ (infant, ado, pregnancy bc muscle growth for example)
    - Inadequate supplies du to : loss Fe in hemorrhage, Dietary deficiency, failure to absorb Fe
    Classification: Microcytic, Hypochromic
60
Q

What is the distribution of iron in our body?

And our daily intake?

A

Total amount = 4g
65% Hb, 30% stored, 5% myoglobin, 1% enzymes

Daily intake in diet : about 15-20 mg

Daily absorption from gut: 1mg for male , 2mg for females

61
Q

How much iron is requiered for normal erythropoiesis?

And released in normal RBC destruction?

A

erythropoiesis requires 25 mg/day

normal RBC destruction releases 25 mg/day :
1mg lost, 24 mg recycled

so 1mg/d (for male) and 2mg fo female is requiered to be absorbed by the guts

62
Q

What are the proportion of iron (Fe) in the blood?

What portion of Fe is lost in blood?

A

1g Hb contains 3.5 mg Fe
and 15g Hb/100mL blood so 50mg Fe/100mL of blood

Menstrual loss = 50 mL blood/month = 25mg Fe

So lose 25mg Fe/month in period + 28mg Fe/months (bc 1mg/day in RBC destruction) = aroung 50 mg/months so 2mg/day for female

63
Q

What is the etiology and classification of Anemia caused by Ineffective Maturation?
(maturation failure anemia)

A

Etiology :
deficiency in vitamine B12 (usually absorption failure) and Folic Acid (usually dietary absence) (both required for synthesis of DNA)

Classification:
Macrocytic, Normochromic

Voirp.145 for vitamine B12 absorption in IF-B12 complex (intrinsic factor has to be secreted)

64
Q

What is anemia caused by survival disorders (Failure to survive)?

A

Etiology (cause):
Congenital:
- Abnormal membrane structure of RBC (less flexible, more fragile, will breakup in narrow capillaries, sphere shape instead of dumb-bell)
- Abnormal Enzyme systems
- Abnormal Hb structure (ex: Thalassemia - deficiency synthesis of globin amino acids)

Acquiered:
- Toxins
- Drugs
- Antibodies

65
Q

What are the 3 general causes of anemia?

A
  • Failure to produce
  • Failure to mature
  • Failure to survive
66
Q

What word describes and accumulation of blood in tissues?

What word discribes the arrest of bleeding?

What mechanisms are included in the primary and secondary responses of this phenom?

A

accumulation of blood in tissues = Hematoma

arrest of bleeding = Hemostasis

Pimary Hemostasis = Vascular response + platelet reponse

Secondary Hemostasis = clot formation

67
Q

What are the 4 steps of hemostasis?

A
  1. Vascular injury
  2. Vasoconstriction
  3. Platelet Plug Formation
  4. Blood Clot Formation (remains until healing has occured)
68
Q

What happens in the Vasoconstriction phase of hemostasis?

A
  1. nervous reflex
    Opposed endothelial cells stick together
  2. myogenic response
    smooth muscle cells in vessel wall respond to injury by contracting
  3. Chemical vasoconstrictors
69
Q

What happens in the Vasoconstriction phase of hemostasis?

A

platelets (white thrombus) form plug to block the blood from flowing out of the constricted vessel

  1. Adhesion
    von Willebrand Factor provoke adhesion and activation
  2. Activaiton and release of cytokines
  3. Aggregation
    Collagen will bind and activate platelets
    Platelets factors are released and attract more platelets
  4. Consolidation
    When platelet clot formed, consolidate by releasing Thromboxane A2, membrane of platelets also releases ADP and serotonin (vasoconstrictors) and von Willebrand Factor releases PF3 (phospholipids)

revoir p.160

70
Q

What is the platelet’s structure?

Who are they produced?

A

2-4um diameter
No nucleus
Many granules –> factors for vasoconstriction, platelet aggregation, clotting, growth, etc.
Many filaments, mitochondria, microtubule, etc.
Life span: 7-10 days
250 000/uL

Pluripotential stem cells –> Committed stem cells (15-20um) (Trombopoietin mostly from liver) –> nucleus divide but doesn’t separate (megakaryocytes, 60-80um) in Bone Marrow –> little fragments with cell membrane and granules break off and go into blood stream

71
Q

What are platelets functions?

A
  1. Release vasoconstrictors
  2. Form Platelets plug
  3. Release Clotting factors
  4. Participate in clot retraction
  5. Promote Maintenance of Endothelial Integrity
72
Q

What is Petechiae?

A

breakup of capillaries under skin = small red/purple spots

73
Q

What can cause an abnormal primary hemostatic response (prolonged bleeding)

A
  1. Failure of blood vessels to constrict
  2. Platelets deficiencies
    - Numerical < 75, 000/uL
    - functional (congenital, acquired)
    *acquiered: Aspirin (in small doses) inhibits synthesis and release of TXA2

PHYG 209 (6 decks)

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