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PHGY 209 > blood > Flashcards

blood Flashcards

1
Q

what is blood

A

highly dynamic tissue
part of cardiovascular system
homogenous red fluid

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2
Q

describe blood conceptions - way blood was thought of historically (7)

A

supporter of life - lifeblood - essential
associated with emotions - bad blood
reflective of relationships - blood brothers
ancient chinese medicine - blood flow linked with energy flow/chi/chee
ancient greece - advocated bleeding as treatment for diseases (the humours, get rid of fluids = get rid of disease)
medieval western medicine - blood inhabited by good and evil spirits (leeches to remove bad)
modern days - carrier of diseases

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3
Q

name the 3 main functions of blood

A

transport
acid-base balance
protection

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4
Q

describe transport (functions of blood)

A

capillaries transport all throughout body
nutrition
respiratory gasses
excretion of wastes - moving them out
hormone transport - many effects on body function
temperature regulation - core of body is warmer and as blood moves to surface = temp regulation

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5
Q

describe acid-base balance (functions of blood)

A

normal pH range = 7.30-7.45
must stay in range or affects structure of protein (denaturation)

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6
Q

describe protection (functions of blood)

A

has rbcs but also wbcs and plasma proteins which fight infection help with clotting and blood loss

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7
Q

describe centrifuged blood

A

55% plasma
buffy layer - negligible made of wbcs and platelets
45% rbcs

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8
Q

what does blood contain

A

extracellular fluid - ecf - plasma
intracellular fluid - icf - fluid inside blood cells

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9
Q

how much of body mass does blood account for

A

~7% of body mass ~ 5L

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10
Q

what is terminology for normal blood volume

A

normovolemia

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11
Q

what is terminology for lower blood volume

A

hypovolemia

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12
Q

what is terminology for high blood volume

A

hypervolemia

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13
Q

what is hematocrit

A

Ht - useful clinical index
the percentage of blood volume occupied by rbcs
Ht = (height of rbc column/height of whole blood column) x 100
normal ~ 45%

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14
Q

what is volume of blood occupied by rbcs

A

~2.25 L

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15
Q

what is volume of blood occupied by plasma

A

~ 2.75L

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16
Q

what is composition of plasma similar to

A

ISF

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17
Q

describe the components that plasma and isf have in common

A

> 90% water
ions = Na+, K+, Ca++, Mg++, Cl-. HCO3-, PO4- ~ physiological saline 0.9% NaCl
nutrients, respiratory gasses and wastes = glucose, aas, lipids, oxygen and co2 - transported in small quantities all over body - exchanged a lot

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18
Q

describe what differentiates plasma and isf

A

proteins - colloids
plasma has large amount ~7%
albumins ~ 60%
globulins ~35%
fibrinogen ~5%

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19
Q

name and briefly describe the ways to separate plasma proteins

A

differential precipitation by salts like ammonium sulphate
sedimentation in ultracentrifuge - bc have different molecular weights
immunological characteristics - which cell surface proteins are expressed
electrophoretic mobility - electrophoresis

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20
Q

define electrophoresis

A

fractionation method based on movement of charged particles along a voltage gradient

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21
Q

describe electrophoresis generally

A

run current through gel/filter paper
proteins at normal pH have excess negative charges
they will go towards anode and migrate towards positive charges
each protein migrates at own characteristic rate

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22
Q

what is rate of migration influenced by in electrophoresis

A

number and distribution of charges and by molecular weight of each protein
heavier = slower to move

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23
Q

using a stain name the proteins found during electrophoresis

A

albumin
globulins - alpha 1, alpha 2, beta, gamma
fibrinogen

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24
Q

describe serum electrophoretic pattern

A

no fibrinogen peak bc using serum and not plasma
it is plasma without clotting factors (easier to work with serum)

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25
Q

describe origins of plasma proteins

A

albumin, fibrinogen, alpha 1, alpha 2 and beta globulins = from liver
lymphoid tissue (lymphatic) makes gamma globulins (antibodies used to fight infection)

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26
Q

what happens when liver is diseased

A

liver is diseased plasma protein levels decrease

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27
Q

describe electrophoretic pattern in renal disease

A

reduced albumin peak
too much permeability at renal tubules and smallest plasma protein (albumin) flows out into urine

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28
Q

describe electrophoretic pattern in bacterial infection

A

peak in gamma globulin bc fighting infection

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29
Q

describe plasma protein properties (protein - shape - molecular weight - concentration)

A

albumin - small globular protein - 69kDa (easiest to lose since small) - 4g
globulins - many shapes - 90-800kDa (heterogenous group) - 2.7g
fibrinogen - fibrous and long and thin - 350kDa - 0.3g

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30
Q

describe role of plasma proteins

A

major role in determining distribution of fluid between plasma and isf compartments by controlling TRANSCAPILLARY DYNAMICS

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31
Q

describe cell membrane

A

between icf and isf
relatively permeable to ions

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32
Q

describe capillary wall permeability

A

between isf and plasma
freely permeable to h20 and ions
impermeable to proteins

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33
Q

describe ionic composition of body fluids

A

ecf can be approximated by 0.9% NaCl solution = 300 mOsm = 6.7 atms ~ 5100 mmHg
pressures important for movement of fluid across capillary wall

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34
Q

describe osmolarity of body fluids

A

NaCl dissociates into 2 ions
9g/L NaCl –> 9/58.5 (mm) = 0.15 M - 2x molarity so ~0.3 Osm = 300 mOsm

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35
Q

describe common characteristic of isf and plasma - also what is the differentiating component

A

0.9% NaCl
300 mOsm
op = 6.7 atm = 5100 mmHg
main source of difference = 7g% of proteins in plasma - wont be able to cross capillary wall and this causes imbalance

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36
Q

for a net flow of water between components (over capillary wall) there has to be…

A

A DIFFERENCE IN OSMOTIC PRESSURE

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37
Q

describe effect of non diffusible solutes

A

contribute to effective osmotic pressure of a solution
plasma proteins = non diffusible so they can exert osmotic effect
effect = colloidal osmotic (oncotic) pressure of plasma (COP)

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38
Q

describe diffusible solutes and their effect

A

DO NOT contribute to osmotic effect since they are equally distributed on both sides of membrane

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39
Q

what happens if COP increases

A

more water will flow into plasma
water wants to go to area with higher solute concentration

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40
Q

what happens if COP decreases

A

more water will flow into isf

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41
Q

what is the major role of plasma proteins

A

across capillary wall there is no protein diffusion
proteins make a major contributor to the COP of a solution

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42
Q

name the 2 major forms of fluid transport across capillary wall

A

flitration and osmotic flow

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43
Q

what determines how much water will flow into or out of capillaries

A

COP of plasma

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44
Q

define bulk flow

A

flow of molecules subjected to a pressure difference
ex: turn on water tap

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45
Q

what does magnitude of bulk flow depend on

A

hydrostatic pressure difference

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46
Q

what is filtration

A

bulk flow across a porous membrane which acts as sieve withholding some particles

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47
Q

describe filtration across capillary wall - generally

A

higher pressure and pushes through things that are the right size
hydrostatic pressure contributes
high-low across membrane

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48
Q

describe the 2 Key Mechanisms for Transport Across Capillaries (Transcapillary Dynamics)

A

1 - filtration = bc fluid in blood vessel is under pressure (heart beats) it tends to push out fluid from inside capillaries into ISF
2 - plasma proteins (restricted to plasma component) tends to pull in or retain fluid inside capillaries
1 & 2 = STARLING FORCES

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49
Q

what is diffusion responsible for

A

exchange of nutrients, gases and wastes across capillary wall

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50
Q

what do starling forces determine

A

distribution of ECF volume between plasma and ISF
proper balance of the starling forces determines the distribution of liquid across capillary wall

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51
Q

what is COP due to plasma proteins

A

25 mmHg of osmotic pressure on plasma side of membrane

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52
Q

describe the simplified circulatory system

A

heart to artery to arterioles to capillary bed to venules to veins back to heart

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53
Q

describe capillary bed

A

all exchange happens here - between plasma and ISF
provides oxygen, nutrients and picks up waste

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54
Q

what is a capillary

A

blood vessel
single layer of endothelial cells
very thin - almost like pores - this is how things diffuse

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55
Q

describe starlings transcapillary dynamics in relation to a capillary

A

heart = 120/80 (contract/relax) - pressure decreases bc friction along the way - reaches arterial end of capillary bp = 35 mmHg, hydrostatic pressure wants to move fluid out into ISF
at venous end - bp = 15mmHg
cop = 25, so +10 from arteriole end and -10 from venous end - it is the opposing force, wants to pull fluid in

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56
Q

describe filtration and osmotic flow in relation to capillary exchanges

A

filtration tends to push out fluid from inside capillaries
osmotic flow tends to pull in or retain fluid inside capillaries

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57
Q

where do capillary exchanges takes place

A

filtration/absorption take place along the whole length of capillary bed and not just at the 2 ends

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58
Q

describe the fluid distributions between the capillaries and lymphatic system

A

~90% of the fluid filtered out is reabsorbed back into capillaries
10% is drained from tissues by lymphatic vessels

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59
Q

describe the blind ended tubules more in depth

A

finger like projections
more permeable than capillary wall
picks up any excess fluid and proteins and returns it back to the central circulation

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60
Q

describe lymphatic vessels

A

a single layer of endothelial cells
highly permeable to all ISF constituents including proteins that leak (picks up and must removes to keep cop in balance)

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61
Q

describe lymphatic vs blood flow volumes

A

total blood flow = 6000L travel through capillaries
volume flittered into ISF = 20L
volume returned by absorption = 17L
volume returned by lymph drainage = 3L

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62
Q

which proteins contribute the most to COP

A

osmotic pressure of solution depends on number of osmotically active particles volume
NOT size, configuration or charge
ex: 1kg steel balls vs 1kg feathers (feathers = more osmotic pressure since more particles)

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63
Q

describe the 2 relationships protein fracture exerts on an osmotic pressure

A

directly related to its concentration in plasma
inversely related to molecular weight of protein

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64
Q

state the COP of the 3 plasma proteins

A

albumin ~20mmHg
globulins ~5mmHg
fibrinogen ~ <1mmHg

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65
Q

name the 4 factors in transcapillary dynamics

A

hydrostatic pressure
COP
capillary permeability
lymphatic drainage

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66
Q

what is edema

A

accumulation of excess fluid in interstitial spaces
decreased venous return

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67
Q

what causes edema (4)

A

increased hydrostatic pressure
decreased plasma protein (COP)
increased capillary permeability
obstruction of lymphatic drainage

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68
Q

describe increased hydrostatic pressure (causes edema)

A

high blood pressure
increases blood pressure at arterial end and venous end, causing no net absorption on the venous end, so it cannot pull in fluids

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69
Q

describe decreased COP (causes edema)

A

ex in liver or renal diseases
causes COP to be equal to pressure on venous end - also causes no net absorption

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70
Q

describe example of edema due to decreased cop

A

failure to synthesize plasma proteins
eg liver disease
severe protein malnutrition - leads to decreased cop and distended abdomen and fluid leakage
KWASHIORKOR

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71
Q

describe increased capillary permeability (causes edema)

A

if capillary wall becomes more permeable (in damage/infection)
plasna proteins escape into ISF where they can exert oncotic effect
COP is lowered from 25–>20, so 5 mmHg ISF OP, causing proteins to move in

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72
Q

describe reduced lymphatic drainage (causes edema)

A

cant bring back that 10% of fluid, so it causes excess fluid in ISF
ex: during breast cancer, can remove some lymphatic tissue and leads to decrease of venous return (edema)

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73
Q

describe example of edema due to obstructed lymphatic drainage

A

elephantiasis
blockage of lymphatic drainage resulting from parasite infestation
filaria nematode - small worms, adult works block the lymphatic return

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74
Q

name the 3 roles of plasma proteins

A

determining distribution of fluid
contribute to viscosity of plasma
contribute to buffering power of plasma

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75
Q

describe determining distribution of fluid (roles of plasma proteins)

A

determines distribution of fluid between plasma and ISF by starling forces controlling transcapillary dynamics

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76
Q

describe contribute to viscosity of plasma (roles of plasma proteins)

A

how thick/how easily something will move
viscosity contributes to blood pressure

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77
Q

describe contribute to buffering power of plasma (roles of plasma proteins)

A

buffering pH - having the right amount of ions
normal pH range ~ 7.4

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78
Q

describe fibrinogen and some globulins (specific plasma protein functions)

A

are essential to clotting

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79
Q

describe gamma globulins (specific plasma protein functions)

A

aka immunoglobulins
provide specific resistance to infection

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80
Q

describe albumin and some globulins (specific plasma protein functions)

A

act as carriers for lipids, minerals and hormones
transport nutrients throughout body - move substances without harming the tissues (ex: iron is toxic, but its transported so it wont hurt the body)

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81
Q

name the process that is not subject to transcapillary dynamics

A

diffusion

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82
Q

what does the buffy layer and red blood cell layer have

A

different types and functions of blood cells

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83
Q

describe the branches of blood cells

A

single precursor in bone marrow (blood cells) can produce:
erythrocytes - rbcs
thrombocytes - platelets
leukocytes - wbcs

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84
Q

describe number, diameter and lifespan of rbcs

A

number = 5x10^6/uL
diameter = 7.2um
lifespan = 120 days

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85
Q

describe number, diameter and lifespan of platelets

A

number = 250000-400000/uL - lower concentration
diameter = 2-3um
lifespan = 7-8 days

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86
Q

describe number, diameter and lifespan of wbcs

A

number = 8000-10000/uL - much lower
diameter = 10-18um = large in size, depends on type
lifespan = hours-years, (eg like memory cells, last and protect for a long time )

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87
Q

what is hematopoiesis

A

all blood cells are derived from a common multipotent (pluripotential) hematopoietic stem cell
one stem cell gives rise to all different blood cell types

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88
Q

name and explain the 3 types of hematopoiesis

A

erythropoiesis = production of rbcs
thromobopoiesis = production of platelets
leukopoiesis = production of wbcs

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89
Q

what are cytokines

A

substances (proteins or peptides) that are released by one cell and affect the growth, development and activity of another cell

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90
Q

what are HGFs

A

Hematopoietic Growth Factors
cytokines that influence the proliferation and differentiate of blood cell precursors

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91
Q

describe hematopoiesis general pattern

A

starts with pluripotential multipotential stem cell - receives stimulus and is induced - self replication –> 3 types of committed stem cells - other stimulants cause them to develop

leukopoiesis –> leukocytes
thrombopoiesis –> platelets
rrythropoiesis –> erythrocytes

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92
Q

hematopoietic stem cells can either…

A

divide or differentiate

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93
Q

are the sites of hematopoiesis the same during every life stage

A

NOOO
depends on the life stage
prenatal and postnatal

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94
Q

describe prenatal hematopoiesis - initial

A

after fertilization the bloods precursors are going to be formed in the yolk sac (blood islands of the yolk sac of the developing embryo)

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95
Q

describe prenatal hematopoiesis - over course of months

A

~1month = production of precursors is gonna take over in the liver and spleen - peak at 5 months
halfway - blood production will start at level of bone marrow

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96
Q

describe postnatal hematopoiesis

A

blood cells are continually produced in the bone marrow

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97
Q

what is bone marrow

A

spongy tissue inside of bones

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98
Q

describe postnatal hematopoiesis

A

at beginning of life - lots of production in distal epiphyses of the long bones - so like the top of the femur
at around 20 this declines and it is taken up by the axial skeleton - for the rest of your life

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99
Q

name parts axial skeleton - where hematopoiesis takes place - 7

A

flat bones of skull
shoulder bones
sternum
vertebrae
ribs
pelvis
proximal epiphyses of long bones

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100
Q

what is main function of rbcs

A

facilitate transport of respiratory gases

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101
Q

describe rbc characteristics - shape

A

biconcave disk - thinner in middle than edges (jelly donut/dumbbell shape)

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102
Q

what is rbc shape due to

A

presence of spectrin = a fibrous protein forming a flexible network linked to cell membranes

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103
Q

what are the advantages of rbc shape - 3

A

form follows function
maximal surface area and minimal diffusion distance - increases efficiency of oxygen and carbon dioxide diffusion
high degree of flexibility - allows rbcs to squeeze through narrow capillaries

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104
Q

what is cbc

A

complete blood count
number of rbcs, wbcs, platelets, hematocrit, hemoglobin concentration - can diagnose diseases and stuff

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105
Q

name and describe the 3 cell sizes

A

normocytic - 7micron size
microcytic - smaller than normal
macrocytic - larger than nornmal

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106
Q

name and describe the 2 cell shapes

A

sickle cell
shperocyte - loses structure and becomes spherical

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107
Q

what is the amount of rbcs in males and females

A

males = 5.1-5.5 x 10^6 / uL
female = 4.5 - 4.8 x 10^6 / uL

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108
Q

what is amount of rbcs in blood

A

~25x10^12 in 5L of blood
huge amount

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109
Q

describe rate of production of rbcs

A

rate of production = rate of destruction ~ 2x10^6 / sec

110
Q

describe rbc composition

A

mostly water
some lipids, proteins and ions
33% hemoglobin

111
Q

what do rbcs not have

A

no subcellular organelles
no nucleus or mitochondria
missing from mature rbc

112
Q

name and describe the 2 important enzyme systems of rbcs

A

glycolytic enzymes –> generate energy (anaerobically) - since no mitochondria so allows to produce energy
carbonic anhydrase –> CO2 transport

113
Q

how many O2 molecules can each Hb bind

A

max of 4O2 molecules

114
Q

what is Hb called when combined with O2

A

oxyhemoglobin - HbO2

115
Q

what is Hb called when O2 is released from it

A

deoxyhemoglobin - DeoxyHb

116
Q

describe hemoglobin structure

A

2 alpha chains, and 2 beta chains
each chain has heme region with iron and heme is where O2 binds
200-300X10^6 molecules / rbc
molecular weight = 64KDa (similar to albumin)

117
Q

what happens to Hb in lungs

A

Hb becomes saturated with oxygen - appears bright red

118
Q

what happens to Hb in tissues

A

oxygen dissociated from Hb - appears dark red

119
Q

name the functions of hemoglobin

A

transport of O2 - reversible binding with Hb
increases O2 solubility in blood (plasma = 0.3mLO2/100mL plasma & blood = 20mLO2/100mL blood)
transport of CO2
acts as buffer

120
Q

describe transport of CO2

A

binds to globulin molecules

121
Q

why have Hb inside rbcs and not dissolved in plasma

A

has effect on plasma viscosity, COP and on loss via kidney
increases viscosity and COP, easily lost through kidney bc small

122
Q

describe hemoglobin values in males and females

A

males = 16g/100mL blood
females = 14g/100mL blood

123
Q

when Hb is fully saturated with O2 each gram of Hb holds how much O2

A

1.34 mL O2

124
Q

O2 carrying capacity of blood is what

A

20mL O2/100mL blood
(15gx1.34mL = 20)

125
Q

name the 5 factors that affect the ability of Hb to bind and release O2

A

temp
ionic composition
pH
pCO2
intracellular enzyme concentration

126
Q

what is rate of erythropoiesis

A

2-3 x 10 ^6 per sec
must be balance by rate of destruction

127
Q

describe pathway of hematopoiesis

A

under influence of different HGFs
can join lymphoid or myeloid stem cells
becomes committed and differentiates and divides to other cell types

128
Q

can the injection of bone marrow stem cells do

A

reconstitute all hematopoietic cell types
repopulates all of them

129
Q

describe rbc precursor proliferation

A

differentiates in myeloid pathway
division and differentiation = 3-5 days
then produces rbcs - in first 24 hours of their production they are called reticulocytes (newborns)
after first 24 hours = rbc
erythropoietin stimulates erythropoiesis

130
Q

describe red cell precursor proliferation steps - 3

A

1 - decrease in size
2 - loss of nucleus and organelles
3 - accumulation of Hb
stem cell = 18um –> erythrocyte = 7um - shape, size and contents change, loses nucleus and all organelles and accumulates Hb

131
Q

what is a reticulocyte

A

newborn blood cell
has not completely gotten ride of subcellular organelles
some ribosomes visible and havent gotten ride of reticulum

132
Q

what is normal reticulocyte count

A

<1%

133
Q

what is reticulocyte index

A

reflects amount of effective erythropoiesis in bone marrow
medical tests - if its like 5% - raises question of why producing so many rbcs

134
Q

describe 2 factors determining amount of rbcs

A

O2 requirements - like training for marathon, increase exercise and production of more rbcs
O2 availability - like at high altitudes, less oxygen availability , higher altitudes = pO2 lower so compensate by producing more O2 bc low availability

135
Q

what is erythropoietin

A

EPO
glycoprotein hormone/cytokine produced mainly by kidney

136
Q

what is stimulus for release of EPO

A

hypoxia - if body senses hypoxia stimulates more EPO –> more rbcs

137
Q

what might cause hypoxia - 3 things

A

decreased rbc count
decreased availability for oxygen to blood
increased tissue demand for O2

138
Q

describe EPO - genetic manufacturing

A

EPO has been purified, sequenced, gene has been clone, and has been produced by recombinant DNA technology
uses = stimulate rbcs for sick ppl, or abuse - increase O2 capacity

139
Q

describe regulation of erythropoiesis (cycle)

A

kidney = sense hypoxia and increases release of EPO –> increased EPO in plasma –> stimulates RBC production in bone marrow –> increases rbc production (tell by seeing reticulocyte count) –> increased oxygen (carrying capacity) in plasma –> back to kidney (senses increased O2, decreases release of EPO) –> none of other steps happen

140
Q

describe regulation of erythropoiesis mechanism

A

negative feedback mechanism - senses high levels and shuts off or senses low levels and turns on

141
Q

describe regulation of erythropoiesis (statement with words)

A

EPO released from kidney with hypoxia stimulates bone marrow to produce more rbcs - maintaining homeostasis!

142
Q

where is EPO synthesized

A

renal cortex

143
Q

what does EPO act on

A

acts on committed rbc precursors
not on pluripotent cells more downstream

144
Q

most of the processes to maintain homeostasis aree…

A

NEGATIVE feedback

145
Q

describe what happens when sever accidental hemorrhage (steps)

A

severe accidental hemorrhage –> less hb available for oxygen transport –> reduced supply of oxygen to kidneys –> increased production and release of epo –> increased rbc precursor production in bone marrow –> increased discharge of young erythrocytes in blood –> more hb for oxygen transport

146
Q

describe erythropoietin action

A

pluripotent stem cell –> committed myeloid stem cell (epo stimulates proliferation - to produce more cells) –> reticulocytes (epo accelerates maturation - helps it move fastser) –> mature rbcs

147
Q

what is effect of testosterone on epo - 2

A

increased released of epo
increased sensitivity of RBC to precursors of epo - they will be stimulated at lower concentration than normal - more sensitive to epo

148
Q

what is effect of estrogen on epo

A

opposite effects of testosterone = why men have more rbcs than women

149
Q

what is life span of rbcs

A

120 days - nothing prolongs rbc lifespan - nothing protecting them so they degenerate over time
during time - each rbc travels equivalent of 300 miles

150
Q

what happens to old rbcs

A

recognized as such - old and damaged - and are removed from circulation by highly phagocytic cells known as macrophages
at level of liver and spleen

151
Q

describe phagocytosis of old rbcs

A

macrophages eat cells - put out pseudopods - finger like projections and engulf old rbc and uses enzymes to break it down
rbc is digested and contents are released

152
Q

where do contents of phagocytized rbcs go

A

they still have valuable materials so constituents are released into cytoplasm to be used

153
Q

what is function of macrophage

A

destruction of rbcs and recycling of components

154
Q

name the 3 main constituents released when rbcs are broken down

A

globulin
Fe
Hb

155
Q

describe globulin (constituents released when rbcs are broken down)

A

break up globulin and free amino acids move into circulation to make new proteins
produces amino acid pool

156
Q

describe Fe (constituents released when rbcs are broken down)

A

iron - toxic in blood, 4 molecules of iron/hb
transferrin allows Fe to move through blood safely
ferritin attaches and can be stored in liver, spleen and gut
if body needs iron - then ferritin releases and Fe can be picked up transferrin again and transported to bone marrow for rbc production

157
Q

describe hb (constituents released when rbcs are broken down)

A

major component to regulate
hb produces heme - heme is not really used - heme is transformed to bilirubin
bilirubin (1mg/dL) = yellow colour (plasma and urine) most is lost in gut
in liver - converted to biliverdin - to gastrointestinal tract and gives feces colour

158
Q

what happens if bilirubin concentration is >1mg/dL

A

jaundice - yellow colouring of skin and eyes
more bilirubin in plasma = everywhere plasma circulated will appear more yellow

159
Q

what is neonatal jaundice

A

excess of rbcs and lots of hemolysis after birth - usually subsides/is monitored
phototherapy treatments can be used

160
Q

name the 3 causes of jaundice

A

excessive hemolysis
liver damage
bile duct obstruction

161
Q

describe excessive hemolysis - causes of jaundice

A

breaking down more blood = more heme to recycle = more bilirubin

162
Q

describe liver damage - causes of jaundice

A

liver cannot process bilirubin and moves into intestines for secretion and piles up - leads to jaundice

163
Q

describe bile duct obstruction - causes of jaundice

A

blocks bile from entering small intestine and backs up in blood and leads to jaundice

164
Q

what is a normal dynamic for rbcs

A

production = destruction

165
Q

what is polycythemia

A

production > destruction of rbcs
overproduction

166
Q

what is anemia

A

production < destruction
not enough rbcs - cannot pick up enough oxygen

167
Q

how to know if normal or abnormal dynamics of rbcs - normal, polycythemia or anemia??

A

use clinical indices = number of rbcs, amount of hb, and hematocrit (easiest)

168
Q

what can look like polycythemia

A

dehydration
less than normal body water = less plasma = appears as polycythemia

169
Q

what can look like anemia

A

fluid retention
makes plasma compartment more full of water

170
Q

what are normal hemoglobin levels

A

16% hb
5-5.5 x 10^6 rbcs/uL

171
Q

what are polycythemia hemoglobin levels

A

> 18% hb
6 x 10^6 rbcs/uL

172
Q

name and describe (gen) the 2 types of polycythemia

A

relative - due to increased plasma volume - relative to water content
absolute - may be physiological or pathological - related to actual amounts of rbcs

173
Q

describe physiological polycythemia

A

secondary effect
occurs due to higher needs for oxygen or lower oxygen availability

174
Q

describe conditions that would cause physiological polycythemia - 4

A

something that increases demand for oxygen

at high altitude
increased physical activity
chronic lung disease
heavy smoking (less ability to absorb oxygen in lungs)

175
Q

describe pathological polycythemia

A

primary effect that can occur due to tumours of cells producing epo & unregulated production by bone marrow

176
Q

describe polycythemia vera ex

A

7-8 x 10^6 rbcs/uL
Ht ~ 70%
due to stem cell dysfunction = unregulated rbc production

177
Q

why is polycythemia a problem

A

increases blood viscosity - will be thicker
slow blood flow can lead to blood clots

178
Q

what is anemia (in words)

A

decrease in the oxygen carrying capacity of blood

179
Q

describe the measurements defining anemia

A

decreased rbc count
- males = <4 x 10^6/uL
- females = <3.2 x 10^6/uL
decreased hb content
- males = <11g%
- females = <9g%

180
Q

how to classify anemia (morphologic)

A

by size (volume) and colour

181
Q

describe sizes (volumes) of morphologic classifications of anemia

A

microcytic = <80um^3 - small
normocytic = 80-90um^3 - normal
macrocyctic = >94um^3 - too large (cells don’t mature well - part of maturing is shrinking and losing size/contents)

182
Q

describe colours of morphologic classifications of anemia

A

hypochromic <33% - less red
normochromic ~33%hb = normal colour, full of
hb
hyperchronic - super packed full and red

183
Q

name the 3 etiologic classifications of anemia

A

diminished production
ineffective maturation
increased rbc destruction/reduced rbc survival

184
Q

what can diminished production (etiological classifications of anemia) be due to - 3

A

abnormality at site of production (bone marrow)
inadequate stimulus
inadequate raw materials

185
Q

describe abnormality at site of production (bone marrow) - in diminished production (etiological classification of anemia)

A

aplastic (hypoplastic) anemia
etiological = unknown, could be exposure to radiation or chemicals or drugs (failure of bone marrow to produce)
classifications = normocytic and normochromic - just not producing enough

186
Q

describe inadequate stimulus - in diminished production (etiological classification of anemia)

A

stimulation failure anemia
etiology = renal disease (less epo production)
classification = normocytic and normochromic (normal but not enough)

187
Q

describe inadequate raw materials - in diminished production (etiological classification of anemia)

A

iron deficiency anemia (most common)
etiology = increased requirement for Fe or inadequate supply of Fe
classification = microcytic and hypochromic (too small - no iron to make hb, no hb so pale and not filled)

188
Q

go into more detail about iron deficiency anemia

A

can happen during period of growth
increased requirement for Fe = during infancy adolescence and pregnancy
inadequate supply of Fe = dietary deficiency, failure to absorb, loss of Fe in hemorrhage (also like ulcers - losing blood to gastrointestinal tract)

189
Q

what is total amount of iron in body + distributions

A

4g
65% Hb
30% stored
5% myoglobin
1% enzymes

190
Q

what is daily intake of iron in diet

A

~15-20mg per day

191
Q

describe absorption of iron (numbers/day)

A

depends on needs of body - usually don’t absorb all iron - just what we need and some stored, don’t want to have too much since it’s toxic

males ~1mgFe/day
females ~2mgFe/day (who menstruate)

192
Q

why do females who menstruate need more iron than men

A

menstrual lose ~ 50mL blood per month
1gHb contains 3.5mg Fe, 15gHb/100mL blood = ~ 50mg Fe - so menstruating females lose 25mg iron per month and need 50mg per = ~2mg/day

193
Q

describe iron use during erythropoiesis and rbc destruction

A

normal erythropoiesis requires 25 mg per day
normal rbc destruction releases 25mg/day - 1mg is lost and 24 is recycled

194
Q

describe infective maturation (etiological classifications of anemia)

A

maturation failure anemia - cells cannot mature fully
etiology = deficiencies of vitamin B12 and folic acid, inadequate supply of iron
classifications = macrocytic normochromic - cell will not mature so they will stay large

195
Q

what are both vitamin B12 and folic acid required for

A

DNA synthesis

196
Q

describe what could cause inadequate supply of iron

A

dietary deficiencies
failure to absorb
loss of iron in hemorrhage

197
Q

what is vitamin B12

A

found only in animal products - usually failure to absorb (sometimes deficiency in vegans)

198
Q

what is folic acid

A

found in leafy greens
usually dietary absence/overcooking veggies

199
Q

describe increased rbc destruction/reduced rbc survival (rbc survival disorders) - (etiological classification of anemia)

A

hemolytic anemias - may be companied by jaundice
etiological = congenital, acquired (drugs, toxin, antibodies)

200
Q

name and describe the 3 examples and sub examples of hemolytic anemias

A

abnormal rbc membrane structure - hereditary spherocytosis - less flexible more fragile, sphere shaped damages membrane and is gotten rid of bc it’s damaged

abnormal enzyme systems - abnormal metabolism

abnormal hb structure - sickle cell, thalassemia (deficient synthesis of globin aa side chains)

201
Q

what is unique about vitamin B12 absorption

A

requires intrinsic factor
intrinsic factor binds to vitamin B12 and allows it be carried to ileum (end of small intestine) to be absorbed - vitamin B12 would be destroyed in gastric acid of stomach if it wasn’t bound to intrinsic factor

202
Q

what would happen if intrinsic factor deficieny

A

causes pernicious anemia
if don’t have factor (ex could be because part of stomach is removed) or are vitamin B12 deficient = not enough vitamin B13 absorption

203
Q

what secretes intrinsic factor

A

released by stomach cells

204
Q

what type of anemia is pernicious anemia

A

infective maturation - maturation failure anemia
classification = macrocytic and normochromic

205
Q

what is hemorrhage

A

blood loss

206
Q

what are the types of blood loss

A

external - blood goes outside the body
internal - into tissues, internal hemorrhage

207
Q

what is a hematoma

A

accumulation of blood in tissues

208
Q

what is hemostasis

A

arrest of bleeding following vascular injury

209
Q

what is hemostasis due to

A

overlapping mechanisms
vascular response
platelet response
clot formation

210
Q

what is primary hemostasis - def

A

begins within seconds of injury
lasts only minutes
sometimes enough to stop bleeding - like for small blood loss via capillaries

211
Q

what mechanisms make up primary hemostasis

A

vascular response - damaged endothelial cells have their own response
platelet response - critical for stopping blood

212
Q

what is secondary hemostasis

A

takes longer
clot formation

213
Q

name and explain the processes of primary hemostasis

A

vascular injury - damaged endothelial cells and blood escapes
vasoconstriction - contracting smooth muscle to decrease diameter of vessel - slow blood flow to help
platelet plug formation - aggregate at site of injury and stops bleeding

214
Q

name and explain the processes of secondary hemostasis

A

blood clot formation - stop permanently

215
Q

describe vascular response

A

vasoconstriction
smooth muscle cells in vessel wall respond to injury by contracting
opposed endothelial cells stick together - they are pushed together
slows blood flow

216
Q

describe platelet response

A

forms white thrombus - platelet plug
further blocks release of blood

217
Q

describe platelet structure

A

2-4um diameter
no nucleus
~250 000/uL - lot less than rbcs
life span: 7-10 days
not real cells - cell fragments - larger cell pinches off

218
Q

describe the many granules of platelet structure

A

factors for vasoconstriction
platelet aggregation / clotting / growth / etc
many filaments
microtubules
mitochondria
SER

219
Q

where are sites of production of platelets

A

same as sites of hematopoiesis

220
Q

describe hematopoiesis - how platelets form

A

pluripotent hematopoietic stem cell –> myeloid stem cell –> megakaryocyte –> platelets

221
Q

describe platelet production pathway

A

pluripotent stem cell –> committed myeloid stem cell (15-20u) –> megakaryocytes (nucleus divides - multilobed) produces granules and cellular organelles (filled with stuff to be released) –> fingerlike projections into blood stream - pinch off and –> platelets

222
Q

where is thrombopoietin from

A

mostly from liver

223
Q

what is the first thing that happens when blood vessel is damaged

A

expose collagen of endothelial cells and outside vessel

224
Q

after collagen is exposed what happens

A

platelets aggregate and stick to collagen - stick part of endothelium allows platelets to adhere

225
Q

what happens after platelets stick to the exposed collagen

A

platelets and endothelium cells secrete von willebrand factor
which takes one end of the collagen and sticks it with platelets - fix together

226
Q

what does adhesion do to platelets

A

changes their properties
membranes become more sticky and allows them to further aggregate - activation

227
Q

what do platelets release after adhesion (excluding von willebrand)

A

ctyokines - thromboxane A2 - consolidation of platelet plug
ADP & serotonin - vasoconstriction
platelet factor 3

228
Q

what factor does platelet aggregation release

A

von willebrand - enhances adhesion –> aggregation

229
Q

what do damaged endothelial cells activate

A

coagulation pathway
releases thrombin = important for production and formation of clot

230
Q

what does exposed collagen bind and activate

A

platelets

231
Q

what do platelet factors do

A

released and attract more platelets

232
Q

what do platelet factors also promote

A

coagulation scheme

233
Q

name the 5 functions of platelets

A

release vasoconstricting agents / cytokines
form platelet plug (white thrombus)
release clotting factors
participate in clot retraction
promote maintenance of endothelial integrity

234
Q

what is petechia

A

small red/purple spots caused by bleeding into skin
due to capillaries and platelets not functioning properly
when dont have enough platelets - small bleeding under skin through capillaries cannot be stopped

235
Q

what does abnormal primary hemostatic response lead to

A

prolonged bleeding

236
Q

what could abnormal primary hemostatic response be due to

A

failure of blood vessel to constrict
platelets deficiencies

237
Q

name/describe the types of platelet deficiencies

A

numerical (numbers)- <75000/uL
functional (functions) - congenital or acquired

238
Q

describe congenital functional platelet deficiencies

A

cannot produce factors
single factor hereditary deficiencies

239
Q

describe acquired functional platelet deficiencies

A

drugs
toxins
antibodies
multifactor deficiencies
targets platelets and makes them stop

240
Q

what does aspirin do

A

in small doses
inhibits synthesis and release of thromboxane A2
- helps prevent clotting during heart attack or to prevent heart attacks

241
Q

what is a blood clot

A

thrombus
rbcs and wbcs are not required
lots of fibers- causes rbcs to be stuck in it but they do not have any function in a clot

242
Q

what is clot formation a function of

A

plasma
no rbcs needed

243
Q

what is clotting activated by

A

injury to blood vessel wall

244
Q

what does clotting result in

A

sequential activation and interaction of a group of plasma proteins/clotting factors

245
Q

describe group of plasma proteins/clotting factors that are activated by clotting

A

act as cofactors or enzymes - activate other factors
in the presence of calcium or some phospholipid agents (for process to take place)

246
Q

name the 3 stages of clotting

A

injury to vessel wall
stage 2 happens in cytoplasm - not visible
clot formation - only visible stage

247
Q

describe step 3 of clotting

A

fibrinogen (important plasma protein in clotting)
in the presence of thrombin its converted to fibrin = forms mesh that makes blood clot

248
Q

describe step 2 of clotting

A

prothrombin activates thrombin
needs calcium
prothrombinase converts prothrombin to thrombin

249
Q

what is intrinsic pathway

A

damage leads to exposed collagen
all components are found in plasma
cascade of activation of factors

250
Q

what is extrinsic pathway

A

tissue factors (protein and phospholipids) released from damaged cell - outside endothelium activates factors and prothombinase
getting something from inside pathway

251
Q

which pathway (intrinsic or extrinsic) is longer

A

Intrinsic = 3-6 mins
Extrinsic = 15-20 seconds

252
Q

describe feed back of prothombinase

A

Positive - generally bad since clot would never stop growing
but clot retraction opposes this and stops it

253
Q

describe the generation of thrombin in extrinsic and intrinsic pathway

A

small amounts of thrombin generated rapidly in the extrinsic pathway are sufficient to trigger strong positive feedback effects - to generate larger quantities of thrombin in the intrinsic pathway

254
Q

name the 3 factors in coagulation

A

calcium
phospholipid
protein plasma factors

255
Q

what is clotting kept in check by

A

inhibitors of platelet adhesion
anticoagulants

256
Q

what is thrombocytopenia

A

deficiency of platelets in blood

257
Q

what is PF3

A

source of phospholipid activity which participates in coagulation

258
Q

what are anticoagulants

A

naturally occurring elements that block one or more of the reactions of the coagulation scheme
prostacyclins and NO

259
Q

give an ex of congenital single factor hereditary deficiency (clotting factor deficiency)

A

factor VIII
hemophilia - inability to form clots
could also have defects in von willebrand factor

260
Q

give an ex of acquired multi factor deficiency (clotting factor deficiency)

A

liver disease - linked to issues with blood clotting
vitamin K deficiency - travels in bile (produced by liver)

261
Q

what is vitamin K

A

cofactor in synthesis of prothrombin VII, IX, X

262
Q

describe clot retraction

A

clot retraction requires contractile protein - thrombosthenin
released by proteins
only damaged endothelial cells are sticky so its usually very localized
clot retracts from sides

263
Q

what is clot lysis

A

fibrinolysis = thrombolysis

264
Q

describe pathway of clot lysis

A

intrinsic proactivators or extrinsic proactivators –> plasminogen activator –> converts plasminogen to plasmin –> converts fibrin to fibrin fragments = clot breakdown

265
Q

describe intrinsic proactivators of clot lysis

A

factor Xlla
endothelial cell factors

266
Q

describe extrinsic proactivators of clot lysis

A

tissue factors

267
Q

what are other ways to stop formation or get rid of blood clots

A

inhibitors of platelet adhesion
anticoagulant drugs
thrombolytic drugs

268
Q

name an inhibitors of platelet adhesion

A

asprin

269
Q

what do anticoagulant drugs do

A

interfere with clot formation

270
Q

name 2 anticoagulant drugs and describe them

A

coumarin - blocks synthesis of functional prothrombin, VII, IX, X
heparin - inhibits thrombin activation and action (heparin is also naturally occurring in blood but is also a drug)

271
Q

what do thrombolytic drugs do

A

promote clot lysis (helps dissolve clot)

272
Q

name 2 thrombolytic drugs

A

tissue plasminogen activator (tPA)
streptokinase

PHGY 209 (19 decks)

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