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ZOOL 463 > Hematology > Flashcards

Hematology Flashcards

1
Q

consider a situation after onset of obstruction in the lymph vessel
a. capillary pressure decreases
b. capillary pressure increases
c. capillary pressure remains unchanged
d. this leads to increased interstitial colloid pressure

A

capillary pressure remains unchanged - related to heart function or blood pressure NOT lymph

and colloid pressure is a function of movement across membrane (affected by proteins)

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2
Q

how does histamine affect colloid pressure?

A

histamine allows the movement of proteins across membrane, thereby increasing colloid pressure

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3
Q

how much of total body weight is water?

A

~70% (~40 L in a 70 kg man)

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4
Q

what does body water volume change with?

A

age, sex, body fat (obesity)

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5
Q

blood volume of water in women vs men

A

5 L in women and 5.5 L in men

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6
Q

under normal conditions, average intake of water is

A

~2.3 L/day

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7
Q

prolonged heavy exercise changes output of water by increasing/decreasing water output in

A

increasing lungs (breathing), sweat (~50x)
decreasing urine

higher total output

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8
Q

2 main fluid compartments and volume in each

A

intracellular (~28 L) and extracellular (~14 L)

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9
Q

what is intracellular fluid?

A

fluid occupying the space within the cells (i.e., cytoplasm)

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10
Q

what is extracellular fluid?

A

interstitial fluid (~11L), plasma (~3 L), and small compartments such as cerebrospinal fluid, intraocular fluid and fluids of the GI tract

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11
Q

interstitial fluid has the same constituents as plasma except

A

large proteins (present at low concentrations in plasma and even smaller concentrations in interstitial fluid)

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12
Q

relative permeability

A

size determines movement and movement determined by osmotic pressure

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13
Q

what is the relationship between molecule size and permeability

A

inverse relationship

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14
Q

average size of pores

A

~6-7 nM

larger in liver (liver is leaky) and smaller in brain

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15
Q

colloid osmotic pressure is also known as

A

oncotic pressure

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16
Q

colloid osmotic pressure is caused by

A

the presence of proteins

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17
Q

osmotic pressure increases when

A

protein concentration increases

this affects the movement of water and volume (i.e., more water creates higher volume) by drawing water to where there is a higher protein concentration

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18
Q

3 major types of proteins in the plasma in order of abundance

A

albumin, globulin, fibrinogen

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19
Q

total oncotic pressure under normal conditions

A

28 mmHg

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20
Q

albumin’s contribution to oncotic pressure

A

21.8 mmHg (most abundant)

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21
Q

fibrinogen’s contribution to oncotic pressure

A

0.2 mmHg (least abundant)

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22
Q

globulin’s contribution to oncotic pressure

A

6.0 mmHg (second most abundant)

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23
Q

albumin

A

most abundant plasma protein and nonspecific carrier protein - increases half-life when bound

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24
Q

globulin

A

proteins with specificity: e.g., specific carrier proteins, enzymes, immunoglobulins

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25
Q

fibrinogen

A

key factor in blood clotting: polymerizes into long fibrin threads during coagulation

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26
Q

fluid movement in/out capillary is affected by

A

starling forces (hydrostatic pressure + oncotic pressure)

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27
Q

outward pressure on capillaries is determined by

A

capillary pressure = PUSH (blood pressure) + interstitial fluid colloid osmotic pressure = PULL (small amounts of proteins in interstitial fluid)

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28
Q

inward pressure on capillaries is determined by

A

plasma colloid osmotic pressure = PULL (high protein concentration in plasma) + interstitial fluid pressure = PUSH

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29
Q

net force between capillary and interstitial compartment

A

outward force = 28.3 mmHg
inward force = 28.0 mmHg

NET OUTWARD FORCE toward interstitial compartment = 0.3 mmHg - sufficient for small movement from plasma to interstitial fluid

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30
Q

interstitial compartment contains

A

collagen fibres, proteoglycan filaments, interstitial fluid (tissue gel), and free flowing water (~1%)

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31
Q

proteoglycan filaments are made up of

A

98% hyaluronic acid (traps water) and 2% protein

99% of interstitial fluid is entrapped among the proteoglycan filaments, resulting in tissue gel

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32
Q

movement of solutes in the interstitial compartment is by

A

molecular diffusion through the gel (95-99% as fast as in fluid)

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33
Q

conditions that increase fluid in interstitial compartment result in

A

edema (increase the small pocket of free fluid) = swelling due to accumulation of excessive fluid that may result from changes in osmotic colloid pressure

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34
Q

presence of proteoglycan, gel formation and collagen support ensures

A

uniform distribution of fluid within body regardless of body position/gravity, maintenance of optical intracellular distance allowing uniform diffusion of dissolve gases and solutes, mechanical support (giving shape to body parts)

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35
Q

for the lymphatic system, the 0.3 mmHg difference in outward pressure from the capillaries causes

A

fluid movement from capillaries into lymph

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36
Q

is solute concentration higher in arterial or venous blood system?

A

arterial

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37
Q

what does the lymph system use to prevent back flow?

A

1 way valves

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38
Q

lymph system

A

an accessory route for transport of fluid and macromolecules from interstitial space to veins

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39
Q

what do lymph nodes contain and what is their function?

A

contain phagocytic cells and filter lymph to remove foreign blood contaminants before drainage into veins

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40
Q

lymph flow is a function of

A

interstitial fluid pressure

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41
Q

elephantiasis is caused by threadlike filarial worms and leads to lymphedema + necrosis by

A

blockage of lymphatic flow which increases pressure in interstitial compartment, changing starling forces and blood flow

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42
Q

necrosis

A

tissue death - often requires amputation

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43
Q

volume of cerebrospinal fluid

A

150 mL; provides cushioning support for brain

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44
Q

pressure of intraocular fluid

A

15 mmHg; maintains sufficient pressure in eyeball to keep it distended - tightly regulated to prevent glaucoma or blindness

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45
Q

volume of fluid compartment of the GI tract

A

potential space = 15 mL under normal conditions

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46
Q

volume of fluid compartment (pleural cavity) of the lung

A

mucoid fluid = 10 mL - provides lubrication for easy movement of lung

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47
Q

some examples of small fluid compartments

A

pericardial cavity (heart), peritoneal cavity (intestine, stomach, liver), joint spaces, bone and cartilage

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48
Q

haemopoiesis

A

production of blood cells

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49
Q

all blood cells originate from the process of

A

differentiation of pluripotential hemopoietic stem cells

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50
Q

pluripotent stem cells first differentiate into either

A

lymphoid or myeloid stem cells

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51
Q

lymphoid stem cells differentiate into

A

NK cells, B lymphocytes or T lymphocytes

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52
Q

myeloid stem cells differentiate into

A

basophils, eosinophils, neutrophils, monocytes, platelets, erythrocytes (RBC)

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53
Q

once cell is committed, is this process reversible or irreversible?

A

irreversible

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54
Q

what factor controls proliferation and differentiation of blood cells?

A

differentiation factors like cytokines

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55
Q

after stimulation by differentiation factors, the cells are now called

A

committed progenitor cells - destined to become a specific group of blood cells

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56
Q

what 2 things increases production of all haemopoietic stem cells?

A

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

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57
Q

examples of specific differentiation factors

A

erythropoietin, thrombopoietin and granulocytes-monocytes colony-stimulating factors

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58
Q

erythropoietin

A

stimulate differentiation to erythrocytes

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59
Q

thrombopoietin

A

stimulate differentiation to megakaryocytes/platelets

60
Q

granulocytes-monocytes colony-stimulating factors

A

stimulate differentiation to granulocytes and monocytes

61
Q

mature RBC has no

A

nucleus (anucleated)

62
Q

shape of RBC

A

biconcave disk - has deformable membrane

~8 microns diameter and ~1-2 microns in thickness (very narrow)

63
Q

why are RBC so narrow?

A

so they can change shape and pass through small capillaries (soft and squishy to squeeze through narrow cappilaries)

64
Q

RBC constitutes how much of blood volume?

A

48% in males and 42% in females

65
Q

Hematocrit

A

Measure of the proportion of volume that is occupied by red blood cells - determined by centrifugation

66
Q

In severe anemia, hematocrit may decrease to

A

10% (rather than 40-50%) - may result in death

67
Q

Composition of centrifuged blood (parts)

A

Plasma (water, proteins, nutrients, hormones, etc.), Buffy coat (white blood cells, platelets), hematocrit (red blood cells)

68
Q

Anemia vs polycythemia

A

Anemia = depressed hematocrit %
Polycythemia = elevated hematocrit %

69
Q

main functions of erythrocytes

A
  • transport of hemoglobin
  • hemoglobin also acts as an important acid-base buffer for the blood
  • RBC contains carbonic anhydrase which catalyzes production of bicarbonate (important mechanism of CO2 transport)
70
Q

most important oxygen carrier molecule

A

hemoglobin

71
Q

CO2 and water reaction

which is catalyzed by?

A

CO2 + H2O > H2CO3 > HCO- + H+

carbonic anhydrase

72
Q

after birth, RBC are produced by

A

from PHSC in bone marrow but the number of stem cells declines with age

73
Q

relative rates of RBC production in bone marrow in different bones across age

A

RBC produced in all bone marrow at young age

stop producing from tibia and femur by 20-30 and steady decline in vertebra, sternum, and rib

74
Q

committed cells that become erythrocytes (RBC) are called

A

colony forming unit erythrocyte (CFU-E)

75
Q

production of erythrocytes (basic steps)

A

myeloid stem cells (PHSC)
proerythroblast
basophil erythroblast
polychromatophil erythroblast
orthochromatic erythroblast
reticulocyte
mature erythrocyte

76
Q

hemoglobin (Hb)

A

an iron containing molecule (heme) synthesized in erythroblasts

77
Q

hemoglobin subunit is made up of

A

a heme group (4 pyrroles + iron) and a globin (peptide)

78
Q

functional Hb consists of how many Hb subunits (heme + globin)?

A

4 subunits

79
Q

production of hemoglobin

A

succinyl-CoA > pyrrole (repeat for 4 pyrroles)
4 pyrroles > protoporphyrin
protoporphyrin + iron > heme
heme + globin > Hb subunit (4 subunits required for 1 Hb)

80
Q

globin

A

peptide - either alpha, beta, gamma or delta

81
Q

most common form of Hb in adult human

A

Hb A (2 alpha + 2 beta)

82
Q

fetal Hb (Hb F)

A

2 alpha + 2 gamma
has greater affinity for O2 and can carry 20-30% more O2; concentration is 50% greater than adult Hb (outcompetes it)

83
Q

each Hb molecule can carry how many O2 molecules?

A

each iron atom can bind to 1 O2 so each Hb molecule (4 iron atoms) can carry 4 O2 molecules

84
Q

the Fe2+ and O2 bond in Hb is

A

easily reversible (loosely bound)

85
Q

what happens when O2 is bound/unbound to Hb?

A

conformation change when bound/unbound
bound = OXY
when O2 comes off = DEOXY

86
Q

what happens to the conformation of the RBC when O2 comes off in sickle cell anemia?

A

globin crystallizes and forms rigid structure - no longer squishy + causes bursts + leads to anemia (lack of RBC)

87
Q

molecular basis of sickle-cell anemia - difference in the codon for Hb changes

A

amino acid in position 6 from glutamine to valine

88
Q

the specific differentiation factor for RBCs

A

erythropoietin

89
Q

why does kidney removal usually lead to anemia?

A

erythropoietin (differentiation factor for RBC) is a glycoprotein produced mainly in the kidney

90
Q

how does low O2 level affect RBC production?

A

hypoxia stimulates production of erythropoietin which stimulates production of proerythroblasts and RBC

body adapts to low O2 levels by increasing RBC production

91
Q

impaired tissue oxygenation can be caused by

A

low blood volume, anemia, low Hb, impaired blood flow, pulmonary disease, or high altitude

92
Q

what does lack of vitamin B12 or folic acid (B9) lead to?

A

reduced DNA synthesis and failure of nuclear maturation which impairs the formation of RBCs

cells cannot progress from the G2 growth phase to mitosis and enlarge in size causing megaloblastic/pernicious anemia

93
Q

what causes megaloblastic anemia (cells gain size but don’t divide)?

A

impaired absorption of vitamin B12

94
Q

total body content of iron

A

~4 g
65% in the form of hemoglobin and 15-30% stored as ferritin (protein) in liver

95
Q

iron binds to a plasma protein known as

A

transferrin (beta globulin) and forms transferrin-iron complex

96
Q

transferrin-iron complex binds to _____ and does what?

A

receptors on the erythroblasts in the bone marrow and increases the delivery of iron to mitochondria to synthesize heme molecules for hemoglobin synthesis

97
Q

abnormalities in transferrin result in

A

anemia

98
Q

transferrin acts as a control factor of iron absorption from intestine because

A

saturability of transferrin in the blood limits the absorption of iron from GI tract

transferrin > bile > gut > increased iron transport

therefore transferrin increases absorption of iron into circulation

99
Q

average lifetime of RBC

A

~120 days (4 months)

100
Q

if RBC doesn’t have nucleus/organelles, how does RBC form ATP and other compounds?

A

has cellular enzymes capable of limited metabolism to form ATP and other compounds

101
Q

how do RBCs rupture/deteriorate over time?

A

metabolic capability progressively worsens with time resulting in membrane weakening and rupture of RBC particularly in tight spots of the spleen

102
Q

how are damaged RBCs removed?

A

mainly phagocytosed

starts leaking compounds recognized by macrophages (trigger for removal)

103
Q

what happens to iron when damaged RBCs are removed?

A

released iron binds to transferrin for synthesis of new hemoglobin or binds with ferritin for storage

104
Q

what happens to porphyrin (4 pyrroles) in Hb when damaged RBCs are removed?

A

porphyrin is converted to bilirubin which is conjugated and released into blood and bile

105
Q

platelets

A

small fragments of cells shaped like oval discs of 2-4 microns in diameter, derived in the bone marrow from large megakaryocytes

half life = 8-12 days (short)

106
Q

megakaryocytes

A

giant cells with multiple copies of DNA in the nucleus

edges break off to form cell fragments (platelets)

107
Q

platelets contain

A

surface glycoprotein (surface receptors) that recognize tissue matrix protein (i.e., collagen) and damaged endothelial cells

108
Q

platelets do not have a

A

nucleus

109
Q

what causes platelets to contract?

A

actin, myosin and thrombosthenin

110
Q

how are platelets able to make enzymes and store calcium?

A

residuals of both endoplasmic reticulum and Golgi apparatus

111
Q

platelets have _____ to produce ATP and ADP

A

mitochondria and enzymes

112
Q

platelets have an enzyme system to produce

A

eicosanoids (Thromboxane A2)

an activation molecule for platelet recruitment

113
Q

platelet cytoplasm contains _____ for injury-damaged tissue growth

A

fibrin-stabilizing factor + a number of growth factors

114
Q

haemostasis (prevention of blood loss) involves

A

vascular spasm/constriction (limits blood flow from small vessels)
formation of platelet plug
blood coagulation
growth of tissue to repair the injury (once blood loss has stopped)

115
Q

haemostasis

A

stopping blood loss

116
Q

vascular constriction during hemostasis results from a cut or rupture of a blood vessel due to

A
  • local myogenic spasm - partially stimulated by thromboxane A2 (eicosanoid) released by platelets
  • nervous reflex - initiated by activation of pain receptors
117
Q

upon contact with damaged vascular endothelium (i.e., collagen), the surface glycoprotein receptors are activated and result in

A

platelet cell activation

118
Q

what causes other platelet cells to be activated?

A

once activated, platelets produce ADP and thromboxane A2 which activate other platelet cells

119
Q

release of ADP and thromboxane A2 in platelet activation pathway

A
  1. platelet contact with collagen
  2. platelet activation (releases ADP)
  3. breaks down phospholipid (part of membrane) to produce arachidonic acid
  4. arachidonic acid has two pathways: COX-II or lipoxygease
  5. COX-II pathway: produces thromboxane A2
120
Q

platelet activation pathway

A
  1. platelet contact with collagen, activates glycoprotein receptors
  2. activates production of ADP and thromboxane A2
  3. ADP causes swellling and protruding processes that bind other platelets
  4. thromboxane A2 activates other platelets and forms platelet plug + vasoconstriction of blood vessels in area
  5. activated platelets produce fibrin-stabilizing factor, which forms fibrin meshwork + clot
121
Q

what role does aspirin/endomethacin play in blood coagulation?

A

blocks COX-II to prevent production of thromboxane A2

this is why aspirin is used during heart attack to prevent blood thickening/clot formation

122
Q

eicosanoids (thromboxane A2) are derived from

A

phospholipids and then arachidonic acid

123
Q

arachidonic can go through 2 pathways

A

cyclooxygenase-II (COX-II) or lipoxygease

124
Q

prostenoids are formed in the COX-II pathway and include

A

thromboxane, prostaglandins, prostacyclins

125
Q

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

A

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

126
Q

formation of fibrin meshwork and clotting

A

activated platelets produce fibrin-stabilizing factor = forms fibrin meshwork + clotting

127
Q

how does ADP act as a signalling molecule?

A

causes swelling and produces protruding processes that bind to other platelet cells (autocrine and paracrine process)

128
Q

thromboxane A2 leads to formation of

A

a platelet plug - other platelet cells are activated and aggregate to form this

129
Q

why is blood coagulation local?

A

we have a combination of coagulants and anti-coagulants in blood to prevent blood clots forming in unneeded areas

130
Q

blood vessel trauma results in the activation of

A

extrinsic and intrinsic factors leading to the activation of thrombin by releasing tissue prothrombin activator

131
Q

thrombin

A

key enzyme formed by cleavage of prothrombin

thrombin cleaves fibrinogen to form fibrin

132
Q

prothrombin to thrombin

A

in liver due to vitamin K

  1. prothrombin cleaved to fragment 1+2 and prethrombin-2
  2. prethrombin-2 forms thrombin
133
Q

2 roles of thrombin

A

cleaves fibrinogen to form fibrin monomers and activates fibrin-stabilizing factor which polymerizes fibrin threads/meshwork

134
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)

135
Q

what does the fibrin meshwork do at the site of trauma?

A

holds platelets and blood cells together to form the clot and also adheres to damaged surfaces of blood vessel to prevent further blood loss

136
Q

factors that initiate blood coagulation

A

factor III (tissue thromboplastin) and factor XII (Hagemen factor)

137
Q

factor III

A

AKA tissue thromboplastin

initiates extrinsic pathway (lipoprotein + phospholipid); released from tissue following trauma

138
Q

factor XII

A

AKA Hagemen factor

initiates intrinsic pathway; contact of this factor with platelet, collagen or wettable surface results in configuration change + activation which activates other factors and leads to clotting

139
Q

what ion is blood coagulation dependent on

A

calcium

140
Q

extrinsic pathway is initiated by

A

tissue thromboplastin (factor III)

141
Q

intrinsic pathway is initiated by

A

Hageman factor (factor XII)

142
Q

blood coagulation is highly localized because of

A

natural anticoagulants

143
Q

examples of anticoagulants

A

glycocalyx, thrombomodulin, heparin

144
Q

glycocalyx (anticoagulant)

A

mucopolysaccharide absorbed to inner surface of endothelium - repels the clotting factors and platelets

145
Q

thrombomodulin (anticoagulant)

A

membrane protein expressed on the surface of endothelial cells - binds with thrombin and prevents coagulation

146
Q

heparin (anticoagulant)

A

activate other factors that remove/destroy thrombin; also increase activity of antithrombin-III and thrombomodulin by 100-1000 fold (very potent)

ZOOL 463 (4 decks)

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