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PHGY 209 > Blood > Flashcards

Blood Flashcards

1
Q

function of blood

A

Transport
Temp regulation
pH balance
Protection

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2
Q

Components of blood

A

Plasma(55%) of total blood volume
Blood Cells (RBCs-erythrocytes and WBCs-leukocytes)
Cell fragments - platelets

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3
Q

Ht

A

height of RBC column/height of whole blood column times 100 (%)

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4
Q

Plasma composition

A
  1. 90% water
  2. Ions (Na+ and Cl-)
  3. Nutrients
  4. O2 and CO2
  5. Proteins(colloids) = 7g%
    • albumins = 60%
    • globulins = 35%
    • fibrinogen = 5%
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5
Q

Can separate Plasma proteins…

A

Precipitation by salts
Ultracentrifuge (molecular weight diff)
Electrophoretic mobility
Immunological characteristics

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6
Q

Electrophoresis

A

Movements of charged particles along a voltage gradient

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7
Q

Order of Migration and Largest area

A

Albumin, furthest (area is concentration)
Globulins alpha 1,2
Beta migrate
Fibrinogen
Gamma globulin

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8
Q

Serum

A

Plasma w no fibrinogen
Fibrinogen = clotting
Remove for clearer view
ALBUMIN HAS DARKEST THICKEST BAND

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9
Q

Liver produces

A

Albumin
Fibirnogen
aplha 1 and 2 and Beta clubilins

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10
Q

Lymphoid tissue produces

A

Gamma Globulin (antibodies)

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11
Q

Diseased liver…

A

Plasma proteins decrease

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12
Q

Plasma protein concentrations

A

4% albumin
2.7 globulins
0.3 fibrinogen

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13
Q

ISF and PLASMA composition have…

A

Na+ Cl- and HCO3-

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14
Q

Plasma is different how?

A

7 g% proteins

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15
Q

Plasma proteins….

A

determine the distribution of fluid between ISF and Plasma compartments

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16
Q

Osmotic Pressure

A

Pressure required to stop water from diffusing through a membrane by osmosis

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17
Q

Diff in osmotic pressure allows water to move

A
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18
Q

ONLY non-diffusable solutes contribute to the osmotic pressure of a solution so…

A

PLASMA PROTEINS EXERT osmotic effect

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19
Q

Colloidal Osmotic Pressure

A

Osmotic pressure exerted by Plasma proteins
25 mmHg

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20
Q

W/o COP Plasma and ISF rest at

A

5100 mm Hg

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21
Q

COP increase

A

More water will move into Plasma

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22
Q

COP decrease

A

More water will go into ISF

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23
Q

Proteins don’t diffuse through capillary wall, only water can therefore COP

A
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24
Q

2 forms of fluid transport across capillary wall

A

COP
BULK FLOW

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25
Q

Bulk Flow

A

Flow of molecules subjected to a pressure difference
Bulk flow magnitude = hydrostatic pressure diff
Bulk flow acts like a filter/sieve
Favours fluids to move into ISF

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26
Q

Starling Forces

A

Keep the 3:1 ISF:Plasma ratio 15:5

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27
Q

Starling forces

A

FILTRATION of bulk flow -> pushes fluid OUT of capilliries (into ISF)
Osmotic flow (COP) -> pulls fluid INTO capillaries (into plasma)

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28
Q

Capillaries

A

Only place where exchanges b/w plasma and ISF occur

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29
Q

Heart contraction:

A

120 mm Hg pressure

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30
Q

When blood from ocntraction reaches capillary:

A

35 mm Hg

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31
Q

Filtration - Arterial end

A

Fluid exits capillary since capillary hydrostatic pressure is greater then COP

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32
Q

Venous end

A

Fluid reenters the capillary since hydrostatic pressure is less then blood colloidal osmotic pressure (25 mm Hg)

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33
Q

Hydrostatic pressure

A

Pressure exerted by fluid in vessel

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34
Q

C

A

Capillary hydrostatic pressure -> Forces fluid out of capillary
COP -> Forces fluid into capillary

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35
Q

NET filtration: hydrostatic pressure>CC

A

BP - COP = Net filtration

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36
Q

NET absorbtion: hydrostatic pressure < CC

A

BP - COP = Blood absorbtion ( negative)

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37
Q

Mid capillary

A

No movement bc COP = 25 mm Hg (BP)

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38
Q

Filtration

A

push OUT of capillary -> into ISF, bulk flow

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39
Q

Osmotic flow:

A

Pull INTO capillary, from ISF, COP

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40
Q

90% of fluid filtered out is absorbed back into the capillary

A

10% is drained by the lymphatic vessels
Ultimately returned to circulation

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41
Q

Lymphatic vessels

A

HIGHLY permeable to all ISF components

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42
Q

If 20 L filtered out of capillary into ISF and 17 L brough back then…

A

3L volume is returned by lymph drainage

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43
Q

Osmotic pressure

A

NUMBER of osmotically active particles/ unit volume

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44
Q

Osmotic pressure of plasma protein

A

Directly related to its CONCENTRATION in the plasma
Inversely related to molecular weight (higher molecular weight = lower osmotic pressure)

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45
Q

Albumin = smallest weight

A

therefore HIGHEST COP
molecular weight: 69
concentration: 4g%
COP: 20 mm Hg
controls fluid shifts across capillary wall

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46
Q

Edema

A

excess fluid in ISF
- more fluid in ISF, less fluid in plasma

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47
Q

Causes of Edema: Increase in capillary hydrostatic pressure

A

Normal: 120-35
Edema: 120-55
Therefore 30 mm Hg net filtration out
0 net absorption IN?

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48
Q

Decrease in plasma proteins - decreased COP

A
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49
Q

Increased capillary permeability

A

if capillary wall more permeable plasma proteins can escape into ISF
can exert an oncotic (COP) effect
Normal: ISf oncotic pressure = 0
edema: 5 mm Hg

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50
Q

Obstruction of Lymphatic drainage

A

Inability to reabsorb the 10% of fluid drained out of capillary into ISF
e.g elephantiasis (parasite infection, filaria nermatode)

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51
Q

Hematopoiesis: blood cells

A

Erythropoiesis: RBCs
Throbopoiesis: Platelets
Leukopoiesis: WBCs

52
Q

Biggest to smallest Blood cells

A

WBCS
RBCs
Platelets

53
Q

Volume of Bloodcells biggest to smallest

A

RBCs
Platelets
WBCs

54
Q

Stem cell way

A

Multipotent hematopoietic stem cells
1) Myeloid (RBC,WBC)
2) Lymphoid
First branching of stem cell gives COMMITTED stem cell, can only do one path (leuhopoiesis, erythropoiesis, thrombopoiesis)

55
Q

Hematopoiesis general pattern

A
  1. Division
  2. Differentiation
56
Q

Cytokines

A

substance released by cell affecting activity of other cell

57
Q

HGFs

A

influence proliferation and differentiation of blood cell precursors

58
Q

Sites of hematopoiesis

A

Prenatal: yok sac, then liver and spleen
Prenatal at 6 months: bone marrow inside spaces of bone
Children: decrease in production in distal long bones
Adult: Axial Skeleton ( flat bones, pelvis, shoulder blades)

59
Q

Erythrocyte

A

Transport gasses b/w lungs and cell
Biconcave disk
Shape is due to SPECTRIN
- fibrous protein forming a flexible network linked to cell membrane
- regulates shape of cell

60
Q

Biconcave shape advantage

A

Maximal surace area, minimal volume
Fick’s law: LARGER SURFACE AREA THEREFORE HIGHER DIFFUSION RATE and THINNER = higher diffusion rate
Flexibility (can squeeze through narrow spaces)

61
Q

Men have more RBC’s then women

A

Rate of production = rate of destruction

62
Q

RBC has no subcellular organelles

A

33% hemolglobin
Water
Lipids, proteins, ions

63
Q

Important enzyme substance of RBC

A

Glycolytic enzyme -> energy generator
can break down glucose, RBC has no mitochondria, anaerobic energy generated
Carbonic anhydrase -> CO2 transport

64
Q

Hemoglobin

A

Each molecule of Hb can bind a maximum of 4 O2 molecules
O2 = OxyHb
No O2 = deoxyHb

65
Q

Hemoglobin structure

A

4 amino acid chains
2 alpha chains, 2 beta
Each chain has pigment mollecule: HEME
HEME has 1 iron associated to it
O2 attaches to the iron
4 hemes = 4 irons = 4O2 can bind
Lungs: Hb becomes saturated with O2 -> appears bright red
Tissues: O2 dissociates from Hb -> appears dark red

66
Q

Hemoglobin Functions

A

Transport O2 - solubility of O2 in plasma is v low so need Hb
Thanks to Hb blood can carry 20 mL O2 / 100 mL blood (minimum to be alive)

67
Q

Why Hb inside cell instead of dissolved in Plasma?

A

Plasma viscosity ( Hb inside plasma would increase viscosity = thicker)
Would make it harder for blood to be pushed along
Plasma COP -> Hb in plasma would produce v high COP which would pulls all the fluid into capillaries
Loss via kidney - Hb is same size as Albumin, would lose a lot fo Hb along with iron attached

68
Q

RBC precursors Proliferation

A

erythropoiesis = production of RBC
Committed stem cell stimulated by cytokine called erythropoietin
- secreted by kidney
division and differentiation from committed stem cell = 3-5 days
Committed stem cell -> reticulocyte
reticulocyte -> RBC takes 24 hours

69
Q

Changes when reticulocyte becomes RBC

A

Decrease in size(RBC is smaller)
Loss of nucleus (RBC has no subcellular organelles, Pyknosis -> condensing of nuceli chromatin in nucleus)
Accumulation of Hb

70
Q

Reticulocytes

A

Still has some ribosomes - used to recognize as young RBC
After 24 hours loses ribosomal material
Normal reticulyte count < 1 %
- reflects amount of effetive erythropoiesis in bone marrow
- if you lose a lot of blood then reticulocyte rate my go up

71
Q

2 factors determining num of RBCs

A

O2 requirements: lots of exercise requires more O2
O2 availability: higher altitudes, need more RBC to carry more O2

72
Q

Pluripotent hematopoietic stem cell -> myeloid stem cell + influence of HGF (erythropoietin) -> reticulocyte -> erythrocyte

A
73
Q

Erythropoitein

A

cytokine, HGF
glycoprotein hormone
stimulated by Hypoxia (low O2)
may result from less RBCs, less O2 in blood or increased tissue demand for O2
MADE IN KIDNEYS

74
Q

EPO gene

A

gene promoting erythropoitein

75
Q

Regulation of erythropoiesis

A

O2 supply decreased -> increased release of erythropoietin by kidneys
increased erythropoin in plasma
produces more RBC in bone marrow
increased Hb supply

76
Q

Testosterone

A

Stimulates the release of erythropoietin
Accounts for higher heamtocrit in males
Refulation of erythropoiesis: negative feedback loop
More O2 available = less erythropoietin released from kidneys

77
Q

Hypoxia

A

Erythropoietin released from kidneys
Stimulates bone marrow to produce more RBC -> maintain homeostasis

78
Q

Erythropoietin Action

A

stimulates commited group of RBC to divide and differentiate
Accelerates maturation of reticulocytes
Acts on specifically commintted cells that produce RBC
Does NOT act on pluripotnet stem cell
Function:
1. stimulate division and differentiation of committed group
2. Accelerate maturation of reticulocutes

79
Q

Testosterone

A

Increases release of erythropoietin
Increases the sensitivity of RBC precursors to erythropoietin

80
Q

Estrogen

A

Decreases the release of erythropoietin

81
Q

Destruction of RBC

A

120 days lifespan
ALWAYS 120 days
Nothing prolongs lifespan
Macrophages phagocytose old RBCs in liver and spleen
Some old RBC hemoluze -> break up of RBC - released into blood stream

82
Q

Phagocytosis of old RBC by macrophage

A

Macrophage extends pseudopods(extension of cytoplasm) around old RBC, endocytose them
Old RBC is digested by enzymes in macrophage - membrane is digested
Release contents into a macrophage cytoplasm

83
Q

RBC pathway

A

erythropoiesis in bone marrow (pluripotent stem cell -> myeloid stem cell + erythropoietin -> reticulocyte -> erythrocyte (RBC)
lasts in blood for 120 days
After 120 days: macrophage phagocytoses old RBC in spleen/liver
Macrophage breaks down RBC: contents released into macrophage cytoplasm can be recycled

84
Q

Recycling phagocytosed RBC contents

A

Globulin portion (protein chains) released into amino acid pool
Iron is released from HEME
transferrin takes iron to FERRATIN which stores iron in the liver, spleen, gut bc IRON alone is TOXIC
When needed, transferrin picks up iron from ferratin, delivers it to bone marrow
Heme Oxidized -> biliverdin
released inro circulation and becomes BILIRUBIN -> gives plasma it’s yellow color
picked up by liver and secreted in liver fluid (bile)
Bilirubin is released in the upper portion of small intestine
Eventually released into colon which gives color to feces

85
Q

Jaundice

A

Concertation of bilirubin in plasma is higher then normal
Adult: non-harmful, possibly liver disease
Infants: excess of blood cell
-may do sever damage, bilirubin
-can penetrate the brain

86
Q

Causes of jaundice

A

Excessive Hemolysis (destruction of RBC) - too much bilirubin released
Hepatic damage (liver damage) - liver doesn’t release bilirubin into small intestine(accumulation of bilirubin)
Bile duct obstruction
- bilirubin released by liver in liver fluid -> bile
carried into the bile ducts
obstructed bile ducts: bile cant flow
Bilirubin accumulates
GALL STONES = may block release of bile

87
Q

Clinical indices

A

num of RBCs
Amount of Hb
Hematocrit: % RBC in blood

88
Q

Hematocrit

A

Normally 45% - relative to plasma

89
Q

Anemia

A

Lower Ht - higher plasma %

90
Q

Fluid retention

A

Retain more fluid so plasma volume = Higher -> Ht = lower

91
Q

Polycethemia

A

Excess production of RBC
Higher Ht = lower plasma %

92
Q

Dehydration

A

Plasma volume is decreased (less fluid) = higher Ht

93
Q

Polycythemia

A

Blood cancer in which bone marrow produces excess of RBC

94
Q

Normal Hb in blood

A

16% g %

95
Q

Plycethemia

A

> 18g%
More RBC means more Hb

96
Q

Causes:

A

Relative -> due to decrease in plasma volume
Absolute: Physiological or Pathological

97
Q

Physiological polycythemia:

A

Caused by increased O2 needs
Decreased O2 availability
High altitudes -> less O2
increased physical activity
chronic lung disease
less O2 can enter -> hypoxia triggers eythropoietin production = more RBC
heavy smoking -> high CO in blood and lower O2, hypoxia triggers erythopoietin production - more RBCs

98
Q

Pathological polycemia

A

tumours of cells producing erythropoietin
unregulated production of RBC by bone marrow
- stem cells in bone marrow go crazy

98
Q

Decreased Hb content

A

Males: less than 11%
Females than 9%
NOrmally: males: 16
Females: 11

98
Q

Anemia

A

Decrease in the O2 carryinbg capacity of blood
Each Hb can carry 4 O2 NORMALLY

99
Q

Problem of Polycemia

A

Increases blood viscosity
Sluggish blood flow
Blood clots

99
Q

Decreased RBC count

A

MalesL less then 4*106 RBC
Women: less then 3.2 * 106 RBC

100
Q

Classification of anemias

A

Size of RBC -
microcytic
Normocytic
Macrocytic
Hb content in each RBC
Normochromic = regular amount of Hb(33%)
Hypochromic = less then 33%
lighter in colo center = transparent
less Hb means less heme pigment

101
Q

Causes of anemia

A

Diminished production
- Stem cells don’t produce enough RBC
Ineffective maturation - reticulocytes dont mature
Increased destruction : more RBC being destroyed then produced

102
Q

Diminished production of RBC reasons:

A

Abnormal site of production - problem in bone marrow
APLASTIC(HYPOPLASTIC) ANEMIA - normocytic, normochromic

Abnormal Stimulus -> erythropoietin not doing it’s job
can be caused by renal disease as kidney does not secret erythropoietin

Inadequate raw materials, poor nutrition - cannot produce RBC
- Iron deficiency anemia
need iron for synthesis of Hb
Causes: Failure to absorb, dietatry, more need, loss of iron in hemmorhage, MICROCYTIC (smaller bc less Hb, cant grow to proper size, hypochromic (less Hb))

103
Q

Iron

A

Women need more bc they lose blood during periods, 2 mg/day to stay in iron balance

103
Q

Normally

A

25 mg iron/ day
RBC destroys 25 mg/iron a day

104
Q

Maturation Failure Anemia

A

Reticulocytes dont properpy mature to RBC
Caused by Vitamin B12 deficiency
Folic acid deficiency
Both needed for normal synthesis of DNA
Macrocytic(large bc reticulocytes are big, normochromic)

105
Q

Folic Acid

A

Yeast and leafy plants
Deficiency means abnormal erythrocyte precursors -> decreased num of RBC
- overcooking veggies, losing folic acid

106
Q

Vitamin B12

A

Required for action of folic acid in DNA synthesis and cell division
Animal products
Deficience -> abonrmal folic acid function -> abnormal erythrocyte precursors -> decreased number of RBC
absorption of B12 needs protein -> intrinsic factor
intrinsic factor deficiency = reduced B12 absorption in ileum of SI
results in pernicous anemia

107
Q

Intrinsic factor helps the body absorb B12, if B12 not absorbed then folic acid cant be used leading to deficiency

A

pernicious anemia

108
Q

Survival disorders -> increased destruction of RBC

A

Hemolytic Anemias
- maybe jaundice
- bilirubin accumulation
Can be congenital (at birth) or Acquired

109
Q

Congenital Hemolytic Anemia

A

Abnormal membrane structure
Hereditary spherocytosis, RBC is a sphere instead of a biconcave disk
Fragile and more likely to be destroyed faster

Abnormal enzyme systems
Abnormal metabolism
More destrution of RBC

Abnormal Hb structure
Hb doesnt function properly
Sickle cell anemia
Thalassemia:
deficient synthesis of globin amino acid chains
Less Hb = hypochromic
More likely to be destroyed

110
Q

Acquired Hemolytic Anemia

A

Toxic
Drugs
Antibodies -> against cell membrane component

111
Q

Hemostasis: arrest of bleeding following vascular injury

A

Primary Hemostasis: platelet respons +vasuclar response
platelets accumulate at site of imjuryy to form a block
prevent great lose
Vasuclar response: smaller vesciles contrict to decrease blood flow

Secondary hemostasis = clot formation blood coagulates

112
Q

Homeostasis procedure

A

Vasoconstriction
Platelet plug formation (temporary)
Blood clot formation (more permanent)

113
Q

Platelet response (white thrombus)

A

Temporary response
Limits blood flow temporarily
Forms platelet plug

114
Q

Platelet

A

Lives 7 days
smaller then rbc (2-4 micrometers)
No nucleus
Many granules
Mitochondria unlike rbc

115
Q

Platelet production

A

Pluripotent stem cell -> myeloid commited stem cell + throbopoietin (LIVER!!!!) -> megakaryocytes in bone marrow -> platelets in blood stream

116
Q

Platelet plug formation

A

Adhesion
Activation and release of cytokines
Aggregation
Consolidation

117
Q

Platelet functions

A

Release vasoconstricting agents:
Seratonin
Thromboxane A2
Release clotting factors PF3 -> thrombin
For platelet plug
Participate in clot retraction
Consolidated blood clod
PArticipate in secondary hemostasis (blood cloot)

118
Q

Aspirin

A

Inhibits synthesis and release of thromoboxane A2
Prevents blood clot formation bc primary hemostasis is inhibited

119
Q

Abnormal primary hemostatic response

A

Prolonged bleeding due to blood vessel failure to contrrict which is a genetic abonormality and platelet deficienies thrombocytopenia

120
Q

Platelet Adhesion inhibitors

A

Aspirin

121
Q

Anticoagulant drugs -> interfere with clot formation

A

cOYMADIN - BLOCKS SYNTHEISS OF PROTHROMBIN , 7, 9 AND 10
Heparin - inhibits thrombin activation + action

122
Q

Thrombolytic drugs -> promote clot lysis

A

Tissue plasminogen activator (t-PA) activates plasminogen -> plasmin to digest fibrin
Streptokinase

PHGY 209 (6 decks)

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