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Physiology > Blood > Flashcards

Blood Flashcards

1
Q

Facts about blood

A
  • 7-8% of body weight
  • present in blood vessels but also in tissues
  • thicker than water
  • blood cells sediment in tube due to gravity or in a centrifuge
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2
Q

functions of blood

A

transport - exchange, O2, CO2, nutrients, waste products, ions, hormones, and heat (maintain body temp)
regulation - ion and pH balance
defence - immune protection
hemostasis

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3
Q

hemostasis

A

process of forming blood clots in the walls of damaged blood vessels and preventing blood loss while maintaining blood in a fluid state within the vascular system
natural mechanism
prevention of blood loss

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4
Q

hematocrit

A

% of total blood volume occupied by packed red blood cells
males have greater hematocrit than females (~47%, ~42%)

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5
Q

separation of blood cells and plasma

A

components of whole blood are separated by centrifuge
plasma ~55%, buffy coat - white blood cells + platelets <1%, red blood cells ~45%

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6
Q

anemia

A

low hematocrit
symptoms: tiredness, out of breath, paleness, brittle nails

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7
Q

polycythemia

A

high hematocrit
blood is more viscous = slower (can strain circulatory system)
an adaptational change when moved from sea level to higher elevation where <O2 sat in air → advantage to carry more O2

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8
Q

blood doping

A

in athletes
boost red blood cells to increase O2 delivery to muscles
adverse consequences

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9
Q

intracellular fluid

A

ICF
fluid inside of cells

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10
Q

extracellular fluid

A

ECF
fluid outside of cell membranes
= plasma + interstitial fluid

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11
Q

interstitial fluid

A

outside blood vessels
interstitial space

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12
Q

plasma

A

non-cellular portion of blood - liquid portion
> 90% water
electrolytes, organic molecules, trace elements, gases
transport (CO2)

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13
Q

plasma proteins

A

albumins, globulins, fibrinogen, tranferrin
made in the liver
functions: distribution of body water, buffering, transport, defence, hemostasis

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14
Q

albumins

A

major contributors to colloid osmotic pressure of plasma; carriers of various substances

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15
Q

globulins

A

clotting factors, enzymes, antibodies, carriers for various substances

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16
Q

fibrinogen

A

forms fibrin threads essential to blood clotting

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17
Q

transferrin

A

iron transport

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18
Q

distribution of body water

A

capillary walls are impermeable to plasma proteins → exert osmotic force across wall that pulls water into the blood

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19
Q

serum

A

plasma contains clotting factors that are used up to form a blood clot → remaining clear portion is serum
= plasma - clotting factors

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20
Q

blood cell types

A

red blood cells (erythrocytes)
white blood cells (leukocytes)
platelets (thrombocytes)

identification based on staining (hematoxylin-eosin) characteristics

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21
Q

red blood cells

A

normal count = ~5 million cells/microL

transport of oxygen

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22
Q

white blood cells

A

normal count = ~6 thousand cells/microL

neutrophils, eosinophils, basophils, monocytes, lymphocytes

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23
Q

platelets

A

normal count = ~2 hundred thousand cells/microL

hemostasis

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24
Q

polymorphonuclear granulocytes

A

neutrophils, eosinophils, and basophils
variation in the nucleus but all have granules in the cytoplasm

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25
Q

neutrophils

A

neutrophilic granules (only nuclei are stained)
40-60% of leukocytes

phagocytes

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26
Q

eosinophils

A

contain granules that stain with acidic dyes
1-4% of leukocytes

defence against parasites

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27
Q

basophils

A

have basophilic granules
<1% of leukocytes

inflammation

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28
Q

monocytes

A

have abundant agranular cytoplasm and large kidney-shaped nuclei
2-8% of leukocytes

phagocyte + immune defence

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29
Q

lymphocytes

A

large round nuclei and little cytoplasm
20-40% of leukocytes
B cells and T cells

immune defence

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30
Q

B cells

A

antibody production
humoral immunity

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31
Q

T cells

A

cellular immunity

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32
Q

hematopoiesis

A

process of formation of blood cells
prenatal hematopoiesis occurs in the yolk sac (early embryo), the fetal liver, and the fetal spleen
postnatal hematopoiesis occurs in the bone marrow

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33
Q

multipotent hemtopoietic stem cell

A

differentiates into progenitor cells: lymphoid stem cell or myeloid stem cell

bone marrow cells with capacity to synthesize any cell

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34
Q

lymphoid stem cell

A

in process of hematopoiesis, form lymphocytes

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35
Q

myeloid stem cell

A

in process of hematopoiesis, can form any other blood cell type
need cytokines to differentiate

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36
Q

stages of hematopoiesis

A

all stem cells begin in the bone marrow
stem cells that become T cells will migrate to the thymus gland before differentiating in the blood
red blood cells, platelets, monocytes, granulocytes, and B cells will differentiate in the blood
B cells and T cells will migrate between the blood and tissues depending on need
monocytes will differentiate to macrophages when move to the tissues
granulocytes can also migrate to the tissues

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37
Q

cytokines

A

(hematopoietins)
small proteins that regulate hemtopoiesis
hormone-like in their mechanism of action
act as growth factors

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38
Q

erythropoietin

A

cytokines that regulate hematopoiesis of erythrocytes (red blood cells

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39
Q

thrombopoietin

A

cytokines that regulate hematopoiesis of thrombocytes (platelets)

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40
Q

erythrocytes (red blood cells)

A

7-8 µm diameter
2-3 µm thickness
~ 5 million/µL
120 day lifespan (short without nucleus)

function in O2 transport
lose nucleus and other organelles during development - small shape, only contains Hb
full of hemoglobin molecules

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41
Q

shape of red blood cells

A

biconcave shape - thicker on outside and thinner in middle = greater surface area:volume ratio → allows greater diffusion - transport of O2
shape makes the cells flexible - can more through blood vessels and capillaries

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42
Q

hemoglobin

A

heme (non-protein) + globin (protein)
responsible for ~99% of total oxygen transport

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43
Q

Hemoglobin A

A

HbA - hemoglobin A
alpha2beta2 form = 2 alpha globin chains + 2 beta globin chains
heme = iron-containing non-protein group
max of 4 ferrous iron molecules contained by heme per hemoglobin molecule

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44
Q

O2 transport

A

hemoglobin binds to oxygen in loose and reversible manner
each ferrous iron (Fe++) combines with one molecule of O2 by process of oxygenation
picked up in lungs and delivered to tissues by blood

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45
Q

oxygen binding and unloading

A

oxyhaemoglobin = relaxed binding structure; open pockets so O2 can bind quickly
deoxyhaemoglobin = tight binding structure; changed conformation of globin chains to prevent other gases binding once O2 has been released

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46
Q

CO inhalation

A

= fatal
hemoglobin can bind to other gases - 200x more affinity for CO than O2
high affinity = tight binding and stays bound

colourless + odourless gas

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47
Q

red blood cell production

A

cytokine erythropoietin
dietary factors
intrinsic factor

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48
Q

erythropoietin

A

produced by cells in kidneys
testosterone helps release and regulation of EPO synthesis = difference in hematocrit between males and females
other hematopoietins also play a role

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49
Q

dietary factors of RBC production

A

iron
folic acid
vitamin B12

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50
Q

erythropoietin regulation of RBC production

A

low O2 delivery to kidneys triggers EPO synthesis
kidneys increase EPO secretion, elevating plasma EPO
circulates in blood to increase production of erythrocytes in bone marrow
increases blood hemoglobin concentration → increased blood O2 carrying capacity
= restoration of O2 delivery

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51
Q

factors that decrease oxygenation

A
  1. low blood volume
  2. anemia (decreased red blood cells)
  3. low hemoglobin synthesis
  4. poor blood flow - decreased heart pumping function
  5. pulmonary disease
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52
Q

decreased tissue oxygenation

A

decreased erythropoietin in kidneys causes increased release
trigger hematopoietic stem cells → proerythroblasts → red blood cells → increased hemoglobin = tissue oxygenation

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53
Q

uptake of iron

A

regulation of iron levels

dietary absorption based on sensors in the small intestine
circulates through blood vessels:
i. plasma iron circulates to all other cells
ii. loss of iron through urine, skin cells, sweat, and menstrual blood
iii. storage in liver: fixed deposit bound to ferritin protein

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54
Q

iron recirculation

A

through blood vessels → bone marrow → erythrocytes → spleen and liver → blood

new erythrocytes released from the blood marrow
old erythrocyte removal in spleen - extract iron from hemoglobin

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55
Q

body iron reserve

A

50%: hemoglobin - broken down from old red blood cells
25%: other iron containing proteins
25%: bound with ferritin in liver

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56
Q

recycling iron from old/damaged red blood cells

A

in spleen
old red blood cells taken up into macrophage by phagocytosis
hemoglobin is braken down into heme and globin

globin → protein broken down into amino acids that are released and either used in metabolism of form new proteins
heme → i. iron moves into blood bound to transferrin - sent either to bone marrow to make new hemoglobin or liver for storage (bound to ferritin) ii. biliverdin (green) → bilirubin (yellow) → moves to liver and forms bile → small intestine - excreted as feces or through blood as urine

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57
Q

folic acid

A

needed for synthesis of thymine (essential for DNA)

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58
Q

Vitamin B12

A

essential for folic acid to work

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59
Q

intrinsic factor

A

protein factor released from cells in lining of stomach

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60
Q

absorption of vitamin B12

A

vitamin B12 from diet is moved to the stomach where it binds with intrinsic factor and forms a complex to be transported to the small intestine
in the ileum (lower small instestine), the complex comes apart and transporters move the B12 out into the blood

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61
Q

anemia

A

decreased oxygen-carrying capacity of the blood due to a deficiency of red blood cells and/or hemoglobin contained in the cells

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62
Q

causes of anemia

A

decreased production of rbc in the bone marrow
hemolytic anemia
hemorrhagic anemia
abnormal hemoglobin production

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63
Q

hemolytic anemia

A

increased destruction of the red blood cells in the body

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64
Q

hemorrhagic anemia

A

increased blood loss leading to loss of red blood cells

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65
Q

factors leading to anemia

A

lack of iron
pernicious anemia
aplastic anemia
chronic kidney disease (reduced levels of EPO)
hemolytic anemia due to abnormal shape of RBC or immune reactions during transfusion
hemorrhagic anemia due to injury, bleeding ulcers, or chronic menstruation
abnormal structure of hemoglobin

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66
Q

pernicious anemia

A

lack of vitamin B12

damage can result in decreased intrinsic factor
autoimmune/inflammatory disease can affect transporters so B12 can’t be absorbed

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67
Q

aplastic anemia

A

damage of bone marrow due to radiation/drugs
not making enough red blood cells

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68
Q

Sickle cell disease

A

abnormal structure of hemoglobin beta globin chain
HbS = a2B*2
single amino acid mutation in B chain
cell membranes of sickle-shaped red blood cells are hard and non-flexible, affecting passage through capillaries → damaged cells = hemolytic anemia
autosomal recessive disease

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69
Q

sickle cell adaptation

A

gene is prominent in regions common to malaria infections
carriers of sickle-cell (heterozygotes) have some sickled cells but are more resistant to malaria

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70
Q

immunity

A

defence: body’s capacity to defend itself
self vs non-self
protect from internal damage signals

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71
Q

non-specific defenses

A

innate immunity
born with
physical barrier + chemicals
- intact skin, enzymes in saliva, tears, mucous
- acidic gastric secretion
- granulocytes and macrophages

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72
Q

specific defenses

A

acquired/adaptive immunity
develop by infections
lymphocytes

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73
Q

white blood cell hematopoiesis

A

development in bone marrow
stem cells → WBC precursors → granulocytes; monocytes; B-cells; (T cell precursors move to thymus + finish development)

emerge from bone marrow to blood vessels
granulocytes
monocytes
B-cells + T-cells = lymphocytes

when needed, move from blood vessels to tissues
granulocytes
monocytes → macrophages
lymphocytes

lymphatic system
lymphocytes can recirculate to blood

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74
Q

innate immunity

A

non-specific; no memory; fast
involve phagocytes: granulocytes and macrophages
complement system

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75
Q

acquired immunity

A

specific; memory; slow
involve lymphocytes
antibodies and cytotoxic molecules

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76
Q

appropriate role of immune system

A

defence against foreign invaders
removal of own old damaged abnormal cells
identify/destroy abnormal/mutant cells

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77
Q

inappropriate role of immune system

A

allergies
autoimmune reaction

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78
Q

allergies

A

exaggerated response to harmless substances
heightened sensitivity

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79
Q

autoimmune reaction

A

attacking own immune system
self vs self

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80
Q

inflammation

A

non-specific innate response to tissue injury
compromised physical barrier - cut, wound, burns, infections

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81
Q

purpose of inflammation

A

destruction of non-self →fibrosis (clotting/scar tissue) → healing

inducers → sensors → mediators

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82
Q

physical characteristics of inflammation

A

redness
swelling
heat
pain

loss of function

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83
Q

redness

A

rubor
increased blood flow
histamine

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84
Q

swelling/edema

A

tumor
increased blood flow
histamine

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85
Q

heat

A

calor
increased blood flow
histamine

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86
Q

pain

A

dolor
pressure on nerve endings
bradykinin and prostaglandin

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87
Q

mast cell

A

in tissues
similar to basophils
granules filled with histamine

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88
Q

vascular events

A

release of inflammatory mediators
increased blood flow
increased permeability of small blood vessels

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89
Q

inflamed vasculature

A
  1. increased blood flow
  2. edema expands extracellular matrix
  3. neutrophil emigration

arteriole and venule dilation
deposition of fibrin and other plasma proteins

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90
Q
  1. increased blood flow
A

causes capillaries to enlarge → both venule and arteriole dilation

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91
Q
  1. edema expands extracellular matrix
A

the single layer of endothelial cells expands = leaky
allows plasma proteins out of plasma = increases osmotic force → swelling

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92
Q
  1. neutrophil emigration
A

neutrophils and monocytes move into the infected area

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93
Q

vascular events - acute inflammation

A

release of histamine
local blood vessels dilate
blood vessels become leaky
accumulation of protein + fluid in extracellular spaces
additional inflammatory mediators are released: bradykinin, prostaglandings, complement proteins

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94
Q

cellular events - acute inflammation

A

resident macrophages entrap and kill pathogens - release chemical signals
increased movement of WBCs (neutrophils and monocytes) into infected area
phagocytosis and destruction of foreign non-self

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95
Q

goal of cellular events - inflammation

A

accumulate leukocytes or WBCs in the inflamed tissue and kill non-self

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96
Q

sequence of cellular events - inflammation

A
  1. margination of WBCs
  2. tethering and rolling of WBCs inside blood vessel
  3. activation of WBCs and endothelial cells
  4. arrest/firm attachment of WBCs to endothelial cells
  5. emigration/diapedesis
  6. chemotaxis of WBCs
  7. recognition of non-self by WBCs
  8. phagocytosis of non-self pathogen by WBCs
97
Q

phagocyte movement

A

rolling adhesion
tight binding
diapedesis
migration

98
Q

chemotaxis

A

ability of WBCs to move against a concentration gradient in response to chemical (chemotactic) factors

chemicals are more concentrated at the site of the pathogen

99
Q

chemotactic factors

A

complement products
chemokines
bacterial products
damaged membrane products - arachidonic acid metabolites

100
Q

role of phagocytes at the site of infection

A

recognition of foreign body
attachment to foreign body
internalization destruction of the ‘non-self- pathogen

101
Q

Pattern Recognition Receptors

A

Toll-like receptors
non-specific
proteins expressed on surface of macrophages
recognition of common patterns

102
Q

opsonization

A

process of opsonin addition to bacteria to enhance attachment and engulfment of pathogen

103
Q

opsonins

A

host factors added to non self
speed up the process of phagocytosis
two types: antibodies and complement proteins

104
Q

engulfment

A

injurious agent surrounded by pseudopods and internalized in a membrane-bound phagocytic vacuole

105
Q

killing by neutrophils

A

3 processes could occur based on what is available
1. oxygen dependent killing
2. oxygen independent enzymatic killing
3. suicidal killing

106
Q

oxygen-dependent killing

A

inside neutrophils
production of oxygen free radicals → oxidative burst

107
Q

oxygen free radicals

A

superoxide anion O2-
hydrogen peroxide H2O2
myeloperoxidase → produces HOCl

108
Q

oxygen-independent killing

A

use enzymes
could be in addition to O2 dependent killing

bactericidal proteins and enzymes
- lysozyme
- lactoferrin
- defensins

109
Q

lysozyme

A

action inside the cell
breakdown contents

110
Q

lactoferrin

A

act in the extracellular space
released outside of neutrophil

binds to iron found in the extracellular space → use up iron so that bacteria cannot grow

111
Q

defensins

A

act outside of cell
poke holes in membrane = bacteria can’t survive

112
Q

suicidal killing

A

outside the neutrophils
NETs - neutrophil extracellular traps

113
Q

NETs

A

neutrophils throw out their DNA to trap particles
once entangled, enzymes are used to destroy it

neutrophils do not survive = suicide killing

114
Q

is inflammation beneficial?

A

yes - short-term

no - long-term
too much killing is bad
neutrophilic killing = destructive and indiscriminate
products produced during phagocytosis are released extracellularly - lysosomal enzymes, oxygen-derived active metabolites

115
Q

complement proteins

A

inactive plasma proteins
involved in innate defence

plasma-derived mediators

116
Q

complement activation

A

3 possible ways to activate system: classical pathway, lectin pathway, alternative pathway

OIL: opsonization of pathogens, inflammatory cell recruitment, lysis of pathogens

117
Q

lysis - killing by MAC formation

A

MAC pokes hole in membrane
activated complement proteins insert into surface of membrane
fluid flows inside = compromise bacterial survival

118
Q

MAC

A

membrane attack complex
collection of activated complement proteins

119
Q

innate defense

A

vascular events result in cellular events

bacteria trigger macrophages to release cytokines and chemokines →
vasodilation and increased vascular permeability cause redness, heat, and swelling →
inflammatory cells migrate into tissue, releasing inflammatory mediators that cause pain

large reserves of neutrophils are stored in the bone marrow and are released when needed to fight infection →
neutrophils travel to and enter the infected tissue where they engulf and kill bacteria - neutrophils die in the tissue and are engulfed and degraded by macrophages

120
Q

primary lymphoid tissues

A

sites of lymphocyte differentiation and education
where lymphocyte synthesis begins

bone marrow
thymus

121
Q

lymphocyte education

A

before the lymphocytes emerge from the bone marrow or thymus, they are educated as to what is foreign

122
Q

secondary lymphoid tissues

A

sites where lymphocytes encounter antigen and become activated

lymph nodes
spleen

123
Q

role of lymphocytes in acquired immunity

A

recognize antigens as foreign
respond to antigens
remember the first encounter with an antigen - memory

124
Q

antigen

A

structure to which specific antibody binds to form a complex

125
Q

antibody

A

globulin class of protein
y shape
recognition molecule on B cells - B cell receptor

2 light chains
2 heavy chains
top of ‘y’ = antigen binding site
bottom of ‘y’ = effector cell binding site - where macrophage binds

126
Q

role of B cells

A

B cells in lymphocytes travel through blood to recognize foreign body
antibodies on cell surface bind to antigens if they match
mitosis of B cells
clonal expansion of match receptor in response to antigen
maturation of B cells into plasma cells → produce antibodies
some B cells become memory cells

127
Q

humoral immunity

A

defence against bacterial infections
antibodies bind to antigens → form complex
opsonization
complement activation
‘direct effects’ →neutralization of toxins

128
Q

antibody neutralization

A

toxic molecules bind to receptors on cell surface → physiological changes = symptoms of illness
antibodies prevent antigens from binding = neutralization
ingestion and destruction by phagocyte of bound antigen

129
Q

cellular immunity - acquired immunity

A

major defence against viruses, cancer, transplants
T lymphocytes: helper T cells, cytotoxic T cells, memory T cells

130
Q

antigen presentation

A

processing:
antigen presenting cell (usually a macrophage) engulfs the antigen and processes it - broken down and loaded into MHC → moved to membrane surface
presentation:
MHC protein attaches to helper T cell receptor - presents the antigen

131
Q

3 signals to trigger immune response

A
  1. APC presents antigen on MHC
  2. expression of co-stimulatory molecules on APC → activate process
  3. cytokine secretion by APC
132
Q

Major Histocompatibility Complex

A

MHC
proteins are present on the membrane of most cells
two types: MHC I and MHC II

133
Q

MHC I proteins

A

present on all nucleated cells

134
Q

MHC II proteins

A

present on specialized antigen-presenting cells (macrophages, dendritic cells)

135
Q

helper T cells

A

antigen presented to helper T cells
produce cytokines that activate cytotoxic T cells and B cells

136
Q

cytotoxic T cells

A

activated by cytokines
clones are carried to all parts of the body via blood
toxic molecules released attack antigen-bearing cells (when bound)
perforin + granzymes

137
Q

perforin

A

facilitates entry of cytotoxic granzymes into cell → induces apoptosis

138
Q

immunological memory

A

measure of antibodies in the body
primary response to antigen = small and slow
decline over time
secondary response to antigen = large and fast
vaccination

139
Q

B cell memory

A

naive cells are first exposed to antigen → small number of activated plasma cells, + memory cells (in lymphnodes)

secondary exposure to antigen causes memory cells to divide → more memory cells + large number of activated cells = lots of antibodies

140
Q

active immunity

A

acquired by exposure to disease or vaccination
self-generated antibodies
acquired in weeks (primary) or days (secondary)
lasts months to years
purpose: combat future infection

141
Q

passive immunity

A

acquired by ingestion of antibodies across placenta or through mother’s breast milk
pre-formed antibodies (in the mother)
acquired immediately
lasts a few weeks
purpose: to combat existing infection

142
Q

necessity of hemostasis

A

balance between pro-hemostatic and anti-hemostatic factors

143
Q

pro-hemostatic factors

A

pro-coagulant factors
prevent blood loss

144
Q

anti-hemostatic factors

A

anti-coagulant factors
keep blood fluid

145
Q

steps of hemostasis

A
  1. vasoconstriction (constrict to prevent blood loss - blood flows to site of injury)
  2. primary hemostasis
  3. secondary hemostasis
146
Q

primary hemostasis

A

platelet plug formation
white thrombus
seal area with collected platelets

147
Q

secondary hemostasis

A

blood clotting/coagulation
red thrombus
gel-like clot

148
Q

platelet origin

A

bone marrow stem cells → megakaryocyte (intermediate cell) → blood

149
Q

megakaryocyte

A

giant cells in the bone marrow
form platelets by pinching off bits of cytoplasm and extruding them into the circulation

150
Q

platelet structure

A

non-nucleated (short life-span)

alpha granules
dense granules
glycogen = energy

actin and myosin
phospholipids

151
Q

alpha granules

A

contain relatively large molecules
- adhesion molecules - von Willebrand factor
- growth factors
- some clotting factors
- cytokines

152
Q

dense granules

A

contain relatively small molecules
- ADP and ATP
- serotonin
- Ca2+

153
Q

Von Willebrand Factor

A

vWF
most important protein
adhesion molecule - has sticky properties

154
Q

platelet plug formation

A

occurs with damage to smaller blood vessels

  1. adhesion of platelets - stick to damaged vessel wall
  2. activation of platelets - change shape, express various receptors, and secrete various substances
  3. aggregation of platelets - attract other platelets; stick to each other to form a plug
155
Q

mechanism of platelet plug formation

A

rupture of blood vessel → collagen is exposed to platelets → adhesion (vWF)
platelets release thromboxane, ADP
fibrinogen binds platelets together

156
Q

receptor expression on platelets

A

expression of fibrinogen receptors → fibrinogen binds to platelets and anchors them together
expression of vWF receptors → vWF polymerizes to collagen and binds to receptors on platelets

157
Q

activated platelets

A

5HT - serotonin
TXA2 - thromboxane A2
ADP - adenosine diphosphate
PL - phospholipid

158
Q

5HT role

A

target blood vessels
vasoconstriction → reduce blood flow = limit damage

159
Q

Thromboxin A2

A

vasoconstriction of blood vessels

further platelet aggregation

160
Q

ADP role

A

further platelet aggregation

161
Q

phospholipid - exposed on platelet surface

A

targets thrombin

162
Q

damage to endothelial cells

A

exposed collagen at site of damage

163
Q

reactions involved in hemostasis

A

injury to a blood vessel exposes collagen and thromboplastin → recruitment of platelets to site of injury
platelets releast 5-HT → smooth muscle contraction + vasoconstriction
collagen activates clotting cascade → activation of thrombin by thromboplastin - converts circulating fibrinogen to fibrin monomers → polymerize and cross link; accumulate with platelets to form clot

164
Q

signaling - mediation of response to blood damage

A

adjacent endothelial cells secrete chemical signals (NO and PGI2)
→ influence platelet aggregation and alter blood flow and clot formation at the affected site
= platelet plug does not continuously expand

165
Q

effects of arachidonic acid metabolites

A

arachidonic acid is generated from phospholipids by phospholipase A2

generation of enzymes in 2 pathways:
1. lipoxygenase pathway
2. cyclooxygenase pathway

166
Q

lipooxygenase pathway

A

initiates inflammation
formation of leukotrienes
occurs before COX pathway

167
Q

cyclooxygenase pathway

A

hemostasis
formation of prostoglandins
COX 1 and 2

168
Q

COX 1

A

enzyme carried in platelets (→ non-nucleated = cannot synthesize new machinery)
generation of thromboxane A2

169
Q

COX 2

A

enzyme carried in endothelial cells (→ nucleated; can synthesize new parts after temporary inhibition)
generation of prostacyclin

170
Q

thromboxane A2

A

pro-hemostatic effect:
vasoconstriction
increased platelet aggregation

171
Q

prostacyclin

A

prostaglandin

anti-hemostatic effect:
vasodilation
decreased platelet aggregation

172
Q

effect of aspirin on hemostasis

A

aspirin causes irreversible inhibition of both COX 1 and COX 2

at low doses of aspirin, COX 2 is favoured
endothelial cells can resume synthesis after temporary inhibition by aspirin

173
Q

secondary hemostasis

A

occurs following a platelet plug formation
cascade of enzyme activation → by proteolutic cleavage
formation of gel-like fibrin clot

174
Q

clotting/coagulation factors

A

plasma proteins
mostly made in the liver

175
Q

factor I

A

fibrinogen

176
Q

factor II

A

prothrombin
need vitamin K for synthesis

177
Q

factor III

A

tissue factor

178
Q

factor IV

A

calcium
not made in the liver

179
Q

factors that need vitamin K for synthesis

A

factor II, IX, and X

180
Q

co-factors

A

help other factors
factor V and VIII

181
Q

key step of blood clotting

A

prothrombin is broken down into thrombin by prothrombinase

thrombin converts fibrinogen to fibrin (insoluble plasma protein)

182
Q

activation of thrombin

A

intrinsic pathway and extrinsic pathway come together to activate a “common activated factor”
→ prothrombinase converts prothrombin to thrombin

vessel damage → exposure of blood to subendothelial tissue → activation of plasma factors by enzymes

183
Q

cascade of plasma enzyme activations

A

requires activated platelets, plasma cofactors, and Ca2+

184
Q

mechanism of blood clotting

A

intrinsic pathway + extrinsic pathway
→ activation of factor Xa
→ common pathway

185
Q

intrinsic pathway

A

“contact activation”
XII → XIIa
activates XIa
+ (Ca2+) → activates IXa
+ VIIIa + (Ca2+) + PL → activates Xa

186
Q

extrinsic pathway

A

tissue damage
activates VIIa and TF
+ (Ca2+) + PL → activates Xa

187
Q

common pathway

A

Xa + Va + (Ca2+) + PL
= prothrombin to thrombin
→ fibrinogen to fibrin
fibrin stabilized by XIIIa + (Ca2+)

188
Q

factor deficiencies: VII

A

severe bleeding
extrinsic pathway = cannot initiate

189
Q

factor deficiencies: VIII

A

severe bleeding
no homeostasis
intrinsic pathway = cannot activate factor X

190
Q

factor deficiencies: XI

A

moderate bleeding
intrinsic pathway = cannot activate factor IX

191
Q

factor deficiencies: XII

A

not involved in initiating intrinsic pathway
= no bleeding problem in vivo
(in vitro = failure to clot)

VII can activate IX (bypass if XII deficient)

192
Q

in vivo blood clotting

A

initiation happens at extrinsic pathway → small amounts of thrombin amplify intrinsic pathway to form large clot

thrombin creates positive feedback in intrinsic pathway
- activation of XI, X, prothrombin → thrombin, and stabilizing fibrin

193
Q

role of thrombin in clotting pathway

A
  1. activation of platelets
  2. conversion of soluble fibrinogen to insoluble fibrin
  3. activation of other clotting factors: V, VIII, XI, XIII
  4. activation of protein C → anticoagulant activity
194
Q

hemophilia B

A

X-linked recessive gene
deficiency of factor IX
less common than hemophilia A

195
Q

hemophilia A

A

deficiency of factor VIII

196
Q

regulation of blood clotting

A
  1. prevention of clot formation where and when it is not required
  2. breakdown of clot as tissue repair occurs (fibrinolytic system)
197
Q

prevention of clot formation

A

natural anticoagulants
thrombin
clinical anticoagulants

198
Q

TFPI

A

tissue factor pathway inhibitor
(extrinsic pathway)
inhibits X a and VII a

natural

199
Q

antithrombin 3

A

inhibits thrombin

natural

200
Q

thrombomodulin

A

changes thrombin activity
activates protein C and S

natural

201
Q

protein C and S

A

inhibit V a and VIII a

natural

202
Q

thrombin as an anticoagulant

A

thrombin bound to thrombomodulin has anti-coagulant activity
activates protein C → inhibition of factor VIIIa and factor Va = inhibit coagulation

203
Q

calcium chelators

A

ex. Na citrate
remove ionized calcium (by binding) = no clotting
works in vitro

clinical

204
Q

heparin

A

increases effect of antithrombin 3 (blocks actions of thrombin)
works in vitro and in vivo

clinical

205
Q

antagonists of vitamin K

A

inhibit synthesis of II, VII, IX, and X in liver
works in vivo

clinical

206
Q

fibrinolysis

A

plasminogen activators
plasminogen → plasmin = in presence of clot, turn insoluble fibrin into soluble fibrin degradation products

207
Q

natural plasminogen activators

A

tissue plasminogen activator
released from endothelial cells
release increased by exercise

208
Q

clinical clot busters / thrombolytic drugs

A

plasminogen activator
used to treat patients with heart attacks

209
Q

tenectaplase

A

thrombolytic drug

210
Q

abnormal hemostasis

A

imbalance of pro and anti hemostatic factors
excessive bleeding/hemorrhage
thrombosis

211
Q

excessive bleeding/hemorrhage

A

failure of hemostatic mechanisms when they are required
1. problems with platelets
2. problems with clotting factors

212
Q

thrombocytopenia

A

damaged bone marrow = not enough platelets
excessive bleeding

213
Q

abnormal platelet function

A

ex. vWF deficiency
excessive bleeding

214
Q

problems with clotting factors

A

hereditary deficiencies (ex. hemophilias)
acquired deficiencies (ex. vit K deficiency)

215
Q

thrombosis

A

formation of blood clot when not required
1. hereditary disorders
2. acquired disorders

216
Q

anti X

A

antibody that binds to X antigen (A, B, or D)

217
Q

antigens of the ABO system

A

present on surface of red blood cells
determine blood types
carbohydrate molecules

218
Q

antibodies of the ABO system

A

usually of the IgM class
naturally occurring antibodies
large molecules

219
Q

RBC type A

A

A antigens and anti B antibodies present in blood

220
Q

RBC type B

A

B antigens and anti A antibodies present in blood

221
Q

RBC type AB

A

A and B antigens present in blood
no antibodies

222
Q

RBC type O

A

anti A and anti B antibodies present in blood
no antigens

223
Q

expression of ABO antigens on RBCs

A

ABO genes code for enzymes of the ABO system
enzymes add on the specific terminal carbohydrate molecules to the surface of RBC
= carbohydrate ABO antigen molecules

224
Q

ex. O gene (ABO system)

A

codes no functional enzyme
RBC does not carry CHO antigen

225
Q

AA or AO genotype

A

blood type = A
A antigens on RBC
anti B antibodies in plasma

226
Q

BB or BO genotype

A

blood type = B
B antigens on RBC
anti A antibodies in plasma

227
Q

AB genotype

A

blood type = AB
A and B antigens on RBC
no antibodies in plasma

228
Q

OO genotype

A

blood type = O
no antigens on RBC
anti A and B antibodies in plasma

229
Q

determining ABO blood type

A

separate blood sample into RBC and plasma fractions
RBCs are mixed with known solution of either anti-A or anti-B antibodies
mixture is observed for RBC agglutination or clumping
O will not agglutinate (no antigens for antibodies to recognize)

230
Q

agglutination

A

surface antigens + opposing antibodies (recognize antigens + bind) → clumping + hemolysis

231
Q

cross-match

A

sample donor blood - RBC antigens are matched to sample recipient blood plasma antibodies
match = no recognition, no binding

232
Q

blood transfusion matches

A

ideally, donor and recipient should match ABO blood type
in emergency, O is a universal donor (but cannot receive from anybody but O); AB is a universal recipient

233
Q

Rhesus system antigens

A

protein molecules
form integral part of RBC membrane
IgG class

D gene codes for D antigen on surface of RBC

234
Q

Rh+

A

D antigen present

235
Q

Rh-

A

absence of D antigen (D gene deletion)

236
Q

mismatched blood transfusion (Rh)

A

Rh- is exposed to Rh+ → develops anti-D antibodies
second exposure → anti-D antibodies will bind to Rh+ RBC and cause clumping + hemolysis

237
Q

rhesus mismatch in pregnancy

A

Rh- mother + Rh+ father
1st child: if Rh+ → born healthy but Rh+ crosses into mother’s blood = anti-D antibodies develop
2nd child: if Rh+ → anti-D crosses placenta and binds to Rh+ antigen in child = HDN

238
Q

hemolytic disease of newborn

A

caused by rhesus mismatch in pregnancy if mother is Rh- and child is Rh+
Rh hemolytic disease
fever, chills, nausea
clotting within blood vessels
hemoglobin in urine

239
Q
A

Physiology (12 decks)

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