Exam 2 Flashcards

1
Q

blood facts

A

only liquid tissue in the body (connective tissue)
8% of body weight (5 liters)
temperature is 100ºF
pH is between 7.35-7.45

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2
Q

functions of blood

A
  1. delivers oxygen and nutrients to tissues
  2. transports metabolic waste (CO2)
  3. transports hormones
  4. maintains body temo
  5. maintains pH (carriers a buffer, bicarbonate, that regulates pH
  6. maintains fluid volume (works with kidneys)
  7. prevents blood loss through clotting
  8. prevents infection with specialized immune cells
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3
Q

components of blood

A

formed elements (46%) and plasma (54%)

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4
Q

erythrocytes

A

red blood cells
-nonliving
-45% of formed elements

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5
Q

function of erythrocytes

A

carry respiratory gases
oxygen and CO2

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6
Q

leukocytes

A

white blood cells
-living
-less than 1% of formed elements

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7
Q

function of leukocytes

A

immunity

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8
Q

platelets

A

fragments of cytoplasm
-nonliving
-less than 1% of formed elements

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9
Q

where are all formed elements produced

A

red bone marrow

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10
Q

blood hematocrit

A

shows the percentage of each component of blood

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11
Q

plasma

A

made of 90% water volume and 10% solutes (proteins, globulins, nitrogenous waste, nutrients, electrocytes)

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12
Q

structure of erythrocytes

A

small
biconcave –> pucker on both sides
anucleate- no nucleus or other organelles
has antioxidant enzymes that get rid of accumulates free radicals

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13
Q

how many RBC do humans have?

A

5 million RBC per milliliter of blood

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14
Q

which sex has more RBC?

A

men- testosterone leads to excess production

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15
Q

how many hemoglobin molecules per RBC

A

250 million

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16
Q

oxygen and heme binding

A

each heme binds to one oxygen, so one hemoglobin molecule has 4 oxygens

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17
Q

how many oxygen molecules per milliliter of blood

A

5 million oxygen molecules

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18
Q

composition of hemoglobin

A

globin protein bound to heme pigmnet
globin is complex protein with more than one subunit
heme is pigment that makes blood red

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19
Q

globin protein subunits

A

4 polypeptide chains:
2 alpha and 2 beta
each subunit binds to one heme pigment

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20
Q

heme pigment composition

A

contains oxygen binding iron
each heme can bind to one oxygen molecule SO each hemoglobin can carry 4 oxygen molecules

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21
Q

oxi-hemoglobin

A

hemoglobin with oxygen bound
makes blood bright red

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22
Q

deoxy-hemoglobin

A

when oxygen is not bound
makes blood dark red

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23
Q

transporter mechanism for moving oxygen throughout the body

A

hemoglobin LOVES oxygen
once oxygen starts binding to hemoglobin, it is easier to bind additional oxygen
-likely to stay completely saturated

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24
Q

carbaminohemoglobin

A

hemoglobin carries some carbon dioxide
20% of CO2 in the blood is bound to hemoglobin (the rest is in plasma)
carbon dioxide doesn’t bind to heme, it binds to amino acids on the globin part

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25
hematopoiesis
the production of blood cells (general process) -occurs in red marrow
26
how much blood is produced per day?
one ounce of blood cells per day each ounce contains 100 billion cells
27
composition of blood cell
varies from day to day -when you are sick, your body produces more WBC -when you work out, your body produces more RBC
28
erythropoiesis
production of red blood cells
29
timing of the process of erythropoiesis
takes 3-5 days and produces about 2 million erythrocytes per second
30
are reticulocytes and erythrocytes living?
no thy have lost their organelles and nucleus
31
erythropoietin in regulating erythropoiesis
when blood is low on oxygen, the kidneys produce this hormone **body monitors oxygen level, NOT RBC count** -has receptors on hemocytoblasts, and initiates their division process
32
testosterone in regulating erythropoiesis
increased muscle mass results in an increased need for blood, and more RBC works through the kidneys by stimulating them to release erythropoietin (do not directly stimulate) *why men have more testosterone than women*
33
B vitamins in regulating erythropoiesis
B12 and folic acid increase RBC
34
why are prenatal vitamins important?
B12 and folic acid increase RBC, when a woman is pregnant she needs to create enough RBC for her and the baby
35
iron in regulating RBC
iron is needed to create hemoglobin (we get it in the food we eat- vegans and vegetarians may have low iron)
36
what happens to iron if we don't need it immediately
it gets stored in cells as ferritin and hemoidesterin -when transported in blood, it is called transferrin
37
how long do erythrocytes last?
last between 100-120 days
38
what happens to old erythrocytes
they ultimately get old and macrophages consume them and break them apart process of breaking down occurs in the spleen
39
what happens as we break down RBC
we recycle their parts -heme is split from globin -iron is stripped off heme and stored as ferritin and hemosiderin -heme is broken down and turned into bilirubin
40
what is bilirubin
heme is broken down and turned into this it is picked up by the liver and used to make bile bile is secreted into the small intestine and breaks down fats pigmnet ultimately fades and is expelled into feces
41
what is globin broken down into
it is a protein- broken down into amino acids and used to make new proteins
42
anemias
low number or abnormal number of red blood cells that reduce the oxygen carrying capacity of the blood
43
polycythemia
overproduction of red blood cells blood has trouble moving through tiny capillaries and blood is a sludge
44
diapedesis
the ability for blood cells to leave the blood vessels and enter into the interstitial fluid **only some WBC can do this so they can function in immunity **
45
leukocytes
complete, living cells with nuclei and organelles display positive chemotaxis- chemically attracted to certain areas 5 total types; some contain granules which store things such an enzymes
46
neutrophils
granulocyte phagocytic cells which function in inflammatory response most numerous of all WBC multi-lobed nucleus 50-70% of all WBC
47
basophils
granulocyte full of histamine (a vasodilator) attact other white blood cells stain very dark 0.5-1% of all WBC
48
eosinophils
granulocytes attack parasitic worms two-lobed nucleus 2-4% of all WBC
49
lymphocytes
agranulocytes function in immunity have a large nucleus; found primarily in lymph tissue 25% of all WBC
50
T-cells
type of lymphocyte that attack virally infected cells or tumors
51
B-cells
type of lymphocyte that secrete antibodies
52
monocytes
agranulocytes largest of all WBC with a u-shaped nucleus they leave the blood stream and become macrophages 3-8% of all WBC
53
leukopoiesis
production of white blood cells hemoblast is stimulated and gives rise to TWO different types of stem cells myeloid stem cells give rise to ALL granulocytes and monocytes lymphoid stem cells give rise to lymphocytes
54
interleukins
chemical messengers usually released when fighting an infection when a cell is atatcked by a virus, it releases these to protect neighboring cells
55
colony-stimulating factors (CSFs)
increases WBC count
56
leukemia
cancerous disorder of white blood cells
57
infectious mononucleosis
increase in agranulocytes caused by exposure to Epstein-Barr virus "kissing disease"
58
leukopenia
decrease in white blood cell production immune system is compromised
59
platelets
anucleated cytoplasmic fragments of megakaryocytes contains granules with clotting factors
60
thrombopoiesis
production of platelets
61
thrombopoietin
a protein which stimulates the production of platelets
62
hemostasis
stop bleeding 1. vascular spasm 2. platelet plug formation 3. coagulation
63
vascular spasm
blood vessels constrict and slow down blood flow hemostasis ALWAYS starts with this step
64
platelet plug formation
platelets aggregate at the site of vascular spasm
65
why do we want limitations to platelet plug formation?
we only want to clot where we need it
66
PGI2 (prostacyclin)
from intact endothelial cells; inhibits platelet adhesion, prevents clotting
67
heparin
from intact endothelial cells, inhibits platelet accumulation, prevents clotting
68
vitamin E quinone
limits clotting from diet, a blood thinner
69
intrinsic pathway to coagulation
series of reactions in which clotting factors are converted to their active forms 13 different clotting factors (you activate one, which activates the next, etc.)
70
extrinsic pathway to coagulation
much quicker in addition to the platelets, the injured tissue itself is also involved in this pathway
71
clot retraction
1. Fibrin mesh starts contracting the clot and the contractile proteins in the platelets allow it to pull the plug together (causes the clot to squeeze) 2. this squeezes out the serum that was trapped inside the clot and the the clot ruptures (facilitates repair) 3. ruptured edges of the vessel come closer together 4. PDGF (platelet derived growth factor) stimulates vessel repair (stimulates regeneration of the damaged tissue)
72
fibrinolysis
1. clot produced plasminogen, which is a plasma protein 2. plasminogen is activated by tissue plasminogen activator (TPA) which is released by newly formed epithelial tissue (plasminogen is activated into plasmin) 3. plasmin digests fibrin
73
clot limiting factors
the chemicals secreted to cause a clot to form don;t just stay at the site of injury, they get released into the bloodstream and circulate away only where we have high concentration of these chemicals do we have clots
74
antithrombin III
inactivates thrombin
75
protein C
inhibits intrinsic pathway events (indirectly inhibits production of thrombin)
76
heparin
produced by intact endothelial cells, enhances activity of antithrombin III and inhibits intrinsic pathway
77
thrombus
stationary blood clot is too large and gets stuck (stays attached) blocks the flow of blood in the vessels
78
embolism
a clot breaks free and travels through the blood stream (mobile clot) gets stuck somewhere else in the body (commonly in heart and brain)
79
thrombocytopenia
pathology reduced platelets in the body (due to sickness/infection)
80
hemophilia
genetic disorder that doesn't allow for the production of one or more clotting factors
81
human blood typing
this is hereditary determined by the presence of agglutinogens that are markers on the surface of RBCs
82
agglutinin
attackers from our body -produce attackers for the markers that we don't have
83
agglutinogen
markers in our own body determines blood type
84
Rh Factor
augments blood type Rh+ or -
85
universal donor
type O- can donate blood to anyone because they don't have any antigens or agglutinogens, so another person's antibodies wouldn't have anything to attack
86
universal recipient
AB+ can receive blood transfusions from all types of blood because the person does not produce any antibodies to attack the transfused blood
87
transfusion reaction
occurs when agglutinins and agglutinogens interact, which leads to clumping and blood no longer circulates well
88
erythroblastosis fetalis (aka hemolytic disease of the newborn)
if a mother is RH- and the father is Rh+ and the baby is Rh+, the the first baby will be fine however, because of the transfer of blood during delivery of the first baby, the mother will be exposed to the baby's blood and will start producing anti-Rh antibodies in all subsequent pregnancies, if the baby is Rh+ , the anti-Rh antibodies in the mother will attack the blood of the embryo resulting in a still birth
89
rhogam
injection that suppresses production of anti-Rh
90
mediastinum
compartment in the middle of the chest where the heart sits
91
base
what we consider the top of the heart
92
apex
the bottom of the heart
93
pericardium
double-walled sac that surrounds the heart
94
fibrous pericardium
functions to attach the heart to the thoracic wall composed of dense irregular connective tissue
95
serous pericardium
made of parietal and visceral layers and the pericardial cavity
96
parietal layer of pericardium
covering of the pericardium
97
visceral layer of pericardium
outermost covering of the heart (directly surrounds heart) also called the epicardium
98
pericardial cavity
filled with fluid to maintain the temperature and produce cushion/reduced friction
99
epicardium
outer layer of the heart made of epithelial tissue
100
myocardium
middle layer of heart made of cardiac muscle tissue
101
endocardium
inner layer of the heart composed of simple squamous epithelial tissue which is antithrombotic (you don't want clots for this reason)
102
atria
at the base of the heart
103
ventricles
at the apex of the heart
104
interatrial septum
splits the right and left atrium
105
interventricular septum
splits the right and left ventricles
106
coronary sulcus
also called the atrioventricular groove runs between the area where the atria become ventricles blood vessels sit here so they don't rub on anything when the heart beats
107
interventricular groove
betwen the right and left ventricles runs diagonal on the front of the heart and vertical on the back *good anatomical point to determine anterior vs posterior*
108
auricles
external extensions of the atria that increase surface area of the atria so they can hold more blood (volume)
109
pectinate muscles
muscles that line the atria
110
fossa ovais
the remnant of the foramen ovale, which closes up as an infant
111
trabeculae carneae
muscles in the ventricular walls
112
papillary muscles
"flat" muscles that extend into each chamber of the ventricles and hold onto the valves have string'like extensions that join with the bell
113
vena cava
attached to the right atrium empty all blood into the right atrium
114
superior vena cava
drains head and neck blood into the right atrium
115
inferior vena cava
drains bottom half of body's blood into the right atrium
116
coronary sinus
empties into the posterior side of the right atrium drains all of the blood that when to the heart muscle itself (specifically the myocardium)
117
pulmonary veins
veins from both lungs that enter into the left atrium **oxygen rich blood**
118
pulmonary arteries
coming out of the right ventricle and to the lungs - sometimes known as the pulmonary trunk, that branches into right and left pulmonary arteries
119
aorta
leaves the left ventricle and carries blood to the entire body
120
human circulation
a two-circuit syste, oxygen-rich blood is completely separated from oxygen-poor blood -this is advantageous and makes the process more efficient
121
two circuit system
each circuit has sites for gas exchange ca;;ed capillary beds one capillary bed in the lungs where we pick up oxygen and leave waste one capillary bed in the body tissue where we deliver oxygen
122
pulmonary circuit
leaves the right side of the body heart to lungs with oxygen poor blood
123
systemic circuit
leaves the left side of the body leaves the lungs and goes to the heart and right side of the body with oxygen rich blood (collects waste from the body)
124
coronary arteries
first branch off the myocardium that supplies blood to the heart muscle itself -these arteries are generally the ones that get plugged with plaque
125
cardiac veins
collect all the blood brought by the coronary arteries and return it to the heart chambers for reoxygenation
126
coronary sinus
cardiac veins drain into this and then into the right atrium
127
anastomoses
connection of blood vessels allows blood to come from multiple sources so if one gets blocked, we still have blood supply
128
atrioventricular valves
open when the pressure of blood in the atrium is higher than the pressure in the ventricles prevents backflow of blood from ventricles to atria
129
tricuspid valve
RIght atrioventricular valve between the right atrium and right ventricle 3 cusps
130
bicuspid (mitral) valve
Left atrioventricular valve between the left atrium and left ventricle 2 cusps
131
cordae tendinae
string-like structures that connect the flaps of the valves to the papillary muscles in the ventricles
132
semilunar valves
located between the ventricles and their corresponding artery, and regulate the flow of blood leaving the heart
133
aortic semilunar valve
between the left ventricle and aorta
134
pulmonary semilunar valve
between the right ventricle and pulmonary artery
135
what do valves regulate
the flow of blood through the heart by allowing pressure gradients to be established -pressure is established due to the asynchronous contraction of the heart (lub dub) -atria beat as a unit, then the ventricles beat as a unit while the atria relax
136
cardiac muscles
has striations uni-nucleated functions through sliding filament action connects exist between desmosomes and gap junctions (intercalated discs) heart functions as a contractile unit
137
intrinsic conduction
cardiac muscle doesn't require a nervous impulse because the heart uses this method of conduction
138
auto-rhythmic cells
non-contractile cells that are "leaky" and have unstable resting potentials have a reduced permeability to potassium (sodium is still leaking in but potassium isn't moving out) causes the cells to depolarize (accumulate positive ion on the inside until reaching threshold) at threshold, calcium channels open up and calcium floods into the cell and causes an action potential and leads to muscle contraction
139
what causes msucle contraction in the heart
calcium!!! causes action potential not sodium
140
sinoatrial node
located at the very top of the heart (right atria; near where the coronary sinus empties) spontaneously generates an action potential known as the "pacemaker" of the heart
141
atrioventricular node
located at the top of the right ventricle; right at the intersection of atria and ventricle; next to the interventricular septum signal from SA node shotos down from here to the Bundle of His (towards the apex)
142
Bundle of His
located in the middle of the heart Branches into the left and right bundle branches (runs down the interventricular septum)
143
bundle branches
travel down the heart from the bundle of his (between the ventricles) transmits signal to the purkinje fibers
144
purkinje fibers
located at the apex, runs up along the sides of the ventricles delivers impulses to papillary muscles (this is why they contract before the rest of the ventricle)
145
cardioaccelatory extrinsic innervation
sympathetic nervous impulses that increase heart rate through depolarization
146
cardioinhibitory
parasympathetic nervous impulses that decrease heart rate through hyperpolarization
147
electrocardiogram (ECG)
graphic recording of the electrical events of the heart **not mechanical, does not tell us if the heart is actively pumping blood**
148
p wave
depolarization of the atrium (time lag so that everything can move to the heart)
149
QRS complex
depolaration of the ventricles and repolaration of the atria are both occuring BUT repolarization of atria is masked because the depolarization of ventricles is MUCH more electrically active
150
what are the fatal irregular heart rhythms?
QRS complex -if ventricles cannot pump, there is no oxygen going to the organs
151
T wave
repolarization of teh ventricles
152
what can an ECG show?
heart rate can be determined by pinking any particular portion of the ECG and determining the time between that point and the next point -diagnose pathologies (fibrillations, location of heart attacks, etc) in the conduction system of the heart
153
lub sound
S1 atrioventricular valves closing
154
dub sound
S2 semilunar valves closing
155
murmus
S3 and S4 backflow of blood due to a problem with a valve -could be functional or non-functional
156
cardiac cycle
one heart beat Systole= contraction Diastole= relaxation We have interchanging systole and diastole of both atria, and systole and diastole of both ventricles - contraction of atria when ventricles are relaxed and contraction of ventricles when atria are relaxed **as chambers contract, they create pressure which moves blood**
157
Average BP on left side of heart
120/80
158
Average BP on right side of heart
24/8
159
Why is blood pressure less on the left?
Less blood is being pumped (only going to lungs which is more delicate so there is less pressure)
160
Cardiac output
Stroke volume multiplies by heart rate - amount of blood that leaves the heart per minute
161
Cardiac reserve
Amount of extra blood that can be pushed through the heart when we need it to be -difference between amount at rest and the Mx amount possible **Average is between 20-25 liters**
162
Stroke volume
End systolic - end diastolic -a mount of blood pushed out of the heart during each beat -difference between the amount of blood in the ventricles before and after they contract (systole)
163
Stretch of cardiac msucle and its affect on stroke volume
Pre-Load -the more blood in the ventricles, the more stretch and the stronger the contraction -causes ejection of more blood
164
What is the stretch of cardiac muscle also called
Starling Law of the Heart
165
Contraction strength affecting stroke volume
Neither pre or after-load -muscle can change its permeability to calcium which causes increase in strength of contraction
166
Arterial pressure
After-load If there is increased pressure in the vessels, the heart can’t push blood out because it has to go from high pressure to low pressure
167
What variable is cardiac output
It is a homeostatic variable -our body likes to keep it pretty much the same * if stroke volume increases for some reason, heart rate usually speeds up and if stroke volume decreases, heart rate usually slows down
168
Parasympathetic nervous system affecting heart rate
Release ACh, which causes hyperpolarization of the sinoatrial node Makes it harder to create a pacemaker potential because it slows it down
169
Sympathetic nervous activation affecting heart rate
Releases norepinephrine, which causes the heart rate to increase Changes activity at the sinoatrial node, so it depolarizes faster Also causes an increase in the contractility of the muscle (contracts with more force)
170
Adrenal medulla production of norepinephrine on heart rate
Releases a adrenaline (norepinephrine and epinephrine) as a hormone Causes a short-lived increase in heart rate
171
thyroxine on heart rate
thyroid gland produces thyroxine which increases cellular metabolic activity (which means a need for increased oxygen and more blood) increased heart rate that lasts long
172
BP changes on heart rate
detected by special receptors called baroreceptors (in our neck) if BP goes up, less blood can get out of the heart so the heart needs to speed up to counteract that
173
ionic balances on heart rate
ionic imbalances can speed up or slow down heart rate depending on what we have
174
age on heart rate
heart rate (cardiac reserve) decreases as you age -> won't be able to raise HR as high when exercising
175
sex on heart rate
difference between genders women have a faster HR than males
176
exercise on heart rate
during exercise, your heart rate goes up (body needs more oxygen) if you continue long term aerobic exercise, your resting HR will decrease
177
temperature on heart rate
heart rate goes up when you have a fever (also when its hotter outside)
178
vagal tone
vagus nerve slows down heart rate with the sympathetic nervous system -without supervision, the sinoatrial node would keepo the heart beating at 100-110 bpm
179
tachycardia
abnormally fast heart rate greater than 10bpm
179
vagal escape
the heart starts racing when it shouldn't be -issue with vagal tone
179
bradycardia
abnormally slow heart rate lower than 60bpm if you're an athlete, then this low is normal
180
congestive heart failure
an umbrella term for anything that causes abnormally low cardiac output
181
coronary atherosclerosis
coronary arteries get clogged from plaque deposits stroke volume decreases, decreased amounts of oxygen delivered to the cardiac muscle --> can't contract like it used to leads to congestive heart failure
182
high blood pressure (hypertension)
diastolic BP greater than 90 heart has to contract with more force to eject the blood, decreases stroke volume and cardiac output
183
myocardial infarction
heart attack- oxygen supply to heart has been eliminated temporarily and the heart loses contractility permanently because lack of oxygen made it become fibrous connective tissue -usually happens to coronary arteries!
183
dilated cardiomyopathy
too much blood in the ventricles for an extended period of time "flabby" ventrciles usually because of too much stretch over time
184
development of the heart
mesodermal origin originates as two separate tubes of endothelial tissue that fuse together into a single chambered heart, 23 days post conception by day 25, early stages of the 4 chambers start to form
185
d-looping
the heart begins to flip upside down in the rightward direction the heart will be in its final orientation at 46 days post conception
186
foramen ovale
a hole in the fetus' heart between the right and left atria through the interatrial septim while in the womb, the embryo completes gas exchange via the mother so no blood needs to be sent to the lungs provides shortcut that allows blood to bypass the pulmonary circuit hole closes at birth and becomes fossa ovalis
187
ductus arteriosus
a connection between the pulmonary trunk and the aorta which provides another shortcut in the embryo blood that did not take the shortcut through the foramen ovale goes to right atrium and is pumped into the pulmonary trunk where it then goes through the connections to the aorta blood that would be going to the lungs goes into the aorta instead and is distributed to the rest of the body
188
ligmentum arteriosum
the ductus arteriosus seals and becomes this after birth
189
valve sclerosis
age related change in heart function deposits accumulate on top of the valve flaps, making them more rigid the valves become less functional because it prevents them from closing all the way, so there is back flow of blood decreased cardiac output (gradual process)
190
decreased cardiac reserve
age-related change in heart function as you age, you lose the ability to have a large cardiac reserve this can be somewhat offset by exercise
191
fibrosis of myocardium
if you fail to use the myocardium, it will begin to atrophy and become non-contractile prevent this by staying active
192
atherosclerosis
age related change in heart function accumulation of plaque (typically cholesterol) along the inside of blood vessels reduces diameter of blood vessels, which changes blood pressure caused by high fat diet, cigarette smoking
193
human circulatory system
we have a closed circulatory system blood ALWAYS stays within the vessels
194
arteries
carry blood away from the heart and generally carry oxygen rich blood (exception is the pulmonary arteries)
195
elastic arteries
closer to the heart, larger in diameter have low resistance walls are rich in elastin (sheets of elastic connective tissue) which allows them to rebound and resist to maintain pressure in the blood Ex. aorta or pulmonary artery
196
muscular arteries
further from the heart and smaller in diameter branch off the elastic arteries and carry blood to the organs have some elasticity but not nearly as much; have smooth muscle in their walls
197
arterioles
branches off of muscular arteries and lead to capillary beds
198
capillaries
these are branches off arterioles tiny, microscopic blood vessels that are one cell layer thick (simple squamous epithelial tissue)
199
where is the site of gaseous exchange
in the capillaries gases in the blood can diffuse out into interstitial space and gases in interstitial space can diffuse into the capillaries based on pressure differences
200
venules
capillaries connect to these
201
veins
venules connect to these retrun blood back to the heart, carry oxyegn poor blood (EXCEPT pulmonary veins) more blood here and lowest pressure here valves assist blood returning to heart
202
lumen
opening in the middle of the vessel that contains the blood
203
tunica interna
inner lining of the vessel which surrounds the lumen composed of simple squamous epithelium cells bind to smooth, flat surface *a continuation of the endocardium
204
tunica media
deep to the tunica interna (middle layer) consists of smooth muscle and elastin really thick in arteries and less thick in veins
205
how is blood vessel diameter controlled
controlled subconsciously through the sympathetic nervous system these impulses cause vasoconstriction absence of sympathetic nervous impulses allows vessels to dilate chemicals like epinephrine from the adrenal medulla also cause constriction
206
tunica externa
outermost layet that is made up of collagen and dense irregular conenctive tissue anchors the blood vessels in place
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vasa vasorum
"blood vessels for blood vessels" tiny little blood vessels that feed into the tunica externa and are only found in large blood vessels
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capillaries
microscopic blood vessels for gaseous exchange small enough so each blood cell goes through single file (makes sure every cell gets oxygen and maximizes diffusion) only have tunica interna layer (one layer makes gaseous exchange more efficient
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continuous capillaries
most common epithelial cells, endothelium is very tightly joined together, have intercellular clefts, must go through walls for exchanges located most places in the body (skin, muscles, etc)
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fenestrated capillaries
has pores called fenestrations that increase permeability across wall of capillary located anywhere in the body that has high absorption and filtration rates Ex. endocrine organs, small intestines, kidneys, digestive tract
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sinusoidal capillaries
have relatively large openings, leakiest type of capillary large molecules/blood can pass through the walls Located in liver (recycles old RBC) and bone (red bone marrow is site of blood cell production)
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capillary bed
allows capillaries to function as a network *microcirculation*
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terminal arteriole
sends blood to capillary bed, can change blood flow by changing its diameter
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metarteriole
branches off from terminal arteriole
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thoroughfare channel
becomes post capillary venule, main middle channel
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postcapillary venule
thoroughfare channel empties into this and this returns blood to the vein
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vascular shunt
combination of metarteriole and thoroughfare channel MUST ALWAYS BE OPEN
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true capillaries
branches off arterioles where gas exchange occurs
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microcirculation
regulates the amount of blood going through the capillary beds
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pre capillary sphincters
right before each of the true capillaries, helps open or close individual capillaries can be partially open to control the amount of blood passing through --> regulates micro-circulation within the body
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artery vs veins: ARTERY
thick walls small lumen thick tunica media low blood volume high blood pressure no valves
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artery vs veins: VEINS
thin walls large lumen thin tunica media high blood volume low blood pressure venous valves
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varicose veins
sitting or standing for long periods of time causes the blood to pool and valves to weaken valves begin to bulge in the veins
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muscular pump
helps get blood back to heart blood vessels run next to skeletal muscle when we contract muscles, they change shape and push against walls of the vessels which pushes blood up in the direction of the heart
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respiratory pump
helps get blood back to the heart as we breathe, we have a change in the pressure of our thoracic cavity as we inhale, blood can slip into the low pressure place close to the heart this pulls it up to the heart
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collateral channels
multiple supply channels that connect to each other (connection is called anastomosis) these go to places that need high blood supply if one channel got blocked, there would still be a path for blood to get there
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blood flow
the amount of blood that is flowing in the body at any given time (always moves from high to low) always takes the path of least resistance flow throughout the system is relatively constant but the flow in a particular area is varied -depends on need of that area (if an organ needs more blood, we dilate vessels going to it and constrict vessels going to other areas
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blood flow and BP
blood flow is directly proportional to differences in blood pressure the greater the difference in pressure, the greater the amount of blood flows from high to low pressure
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blood flow and peripheral resistance
blood flow is inversely proportional to peripheral resistance due to friction -flows more easily with less friction through a large vessel
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blood viscosity affecting peripheral resistance
change in slipperiness through the walls of the vessels effects are individual; relatively constant because we can't alter immediately has a low effect
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vessel length affecting peripheral resistance
longer vessel is greater resistance (larger people have longer vessels) -this causes effects between people but not individually low effect (gradual as you grow)
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vessel diameter affecting peripheral resistance
larger diameter has less friction so it's less resistant arterioles change the most determines blood flow has largest effect- can change instantaneously
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systemic blood pressure
BP decreases continually as we move away from the heart lowest pressure is found in veins that return blood to the heart relatively high in the capillaries because it allows nutrient exchange to occur
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pulse pressure
systolic - diastolic pressure
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mean arterial pressure
pressure propelling blood to the tissues of the bodu- determines where blood goes
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MAP equation
MAP= diastolic pressure + (pulse pressure/3) Ex. 120/90= 120-90= 30 90+ (30/3)= 90+10=100 -use diastolic because if your heart stopped pumping, you would still have diastolic pressure
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blood pressure control
requires integration of many different factors in the body
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alter blood distribution to respond to needs
counteracts a brief fluctuation in BP -changes vessel diameter or closes the entire vessel -can be local (single vessel) or systemic (all vessels constrict) changes
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alter vessel diameter
counteracts brief fluctuations in BP dilation lowers pressure constriction raises pressure -in medulla oblongata, a collection of sympathetic fibers called vasomotor fibers attach to the vessels and cause vasoconstriction using norepinephrine
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vasomotor tone
blood vessels are always in a state of slight contraction
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neural reflex arc
baroreceptors are sensory receptors that monitor blood pressure - they decide when it goes up or down
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when baroreceptor detects increase in BP
1. baroreceptors are activated to start sending a signal to the brain 2. this signal is transferred to the vasomotor center 3. the vasomotor center is inhibited and this causes vessels to dilate. 4. peripheral resistance is reduced and blood pressure goes down
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side effects of activating baroreceptors
1. venus return reduced- amount of blood volume to heart is reduced and decreases cardiac output 2. cardiac output reduced- less blood to be squeezed out of the heart which decreases stroke volume 3. heart rate reduced- more time for heart to beat to maintain cardiac output 4. contractile force reduced- less pressure on the walls and less contractile force 5. MAP declines- decline in blood pressure due to less contraction
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results of side effects of activating baroreceptors
Reduced MAP initiates vasoconstriction - respond to low blood pressure by constricting in attempt to bring pressure back up Increase cardiac output -because heart rate slowed down in response to baroreceptor activation, this allows the heart to fill more before each contraction Blood pressure rises
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chemical reflex arcs
chemoreceptors monitor the carbon dioxide concentration, oxygen concentration, and pH of blood - they detect drop in oxygen level or pH, or increase in CO2
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if the chemoreceptors detect a decrease in oxygen, an increase in CO2, or a drop in pH
1. a signal is sent by the chemoreceptor to stimulate the cardioacceleratory center 2. this causes the heart rate to go up and the signal also goes to the vasomotor center 3. the vasomotor center causes the blood vessels to constrict and blood pressure goes up. As BP increase and the heart beats faster, cardiac output increases 4. increased cardiac output means more blood can go to the body, where it can pick up more oxygen and get rid of CO2.
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epinephrine and norepinephrine as a reflex arc
RAISES BP released by the adrenal medulla cause vasoconstriction and increased cardiac output during times of stress
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atrial natriuretic peptide (ANP) as a relfex arc
LOWERS BP released by atria of the heart vasodilation, increased urine production, decrease in blood volume due to water taken out of the blood
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Antidiuretic hormone (ADH) as a relfex arc
RAISES BP released by the posterior pituitary retains fluids and only causes vasoconstriction when extreme hemorrhage happens
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Angiotensin II as a reflex arc
RAISES BP released by the liver linked to resorption of blood and water via aldosterone production; causes vasoconstriction
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Endothelium-derived factors as a reflex arc
can eitehr raise or lower bp by constricting or dilating released by lining of blood vessels blood vessels release chemicals to change their own diameter
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inflammatory chemicals as a reflex arc
LOWERS BP released by immune system 1. causes inflammation in response to damaged or infected tissue 2. increased permeability of circulatory system so things can leave easily
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Histamine effects on blood pressure
histamine in released during anaphylactic shock and causes a deadly crash in blood pressure
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alcohol as a reflex arc
LOWERS BP 1. inhibits ADH 2. inhibits vasomotor center (leads to vasodilation) 3. directly causes vasodilation
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nicotine as a relfex arc
Raises BP functions exactly the same as epinephrine and norepinephrine
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what is the ONLY long-term mechanism of regulating blood pressure
renal regulation
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how does renal regulation work
alters blood volume, which changes blood pressure lower blood volume=lower blood pressure higher blood volume=higher blood pressure *change in pressure causes kidneys to eliminate more water and produce more renin
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direct renal regulation mechanism
increase in blood pressure or blood volume speeds up filtration rate in the kidneys blood DIRECTLY affects the kidneys increased filtration rate increases blood volume, pressure, and amount of blood delivered by the arteries
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indirect renal mechanism
indirect- involves the liver 1. low blood pressure causes kidneys to release more renin and this stimulates angiotensin II production. this stimulates the adrenal medulla to produce aldosterone 2. aldosterone causes water to be reabsorbed and creates an osmotic gradient. 3. blood follows water back into the bloodstream and blood pressure increases
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pulse
as blood is circulationg, it creates waves of pressure and causes the feeling of pulse -expansion and recoil of arteries
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blood pressure
related to the flow of blood pushing on the vessel wall sphygmomanometer= BP cuff 1st Korotkoff sound= systolic 2nd Korotkoff sound= diastolic
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tissue perfusion
flow of blood is delivered to the body tissues based on need as blood is flowing through tissue it delivers oxygen and nutrients and removes waste as blood passes through the lungs it exchanges gas as blood passes through the kidneys, it forms urine
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changes in tissue perfusion
during exercise: we can increase cardiac output by dipping into our cardiac reserve -do this by increasing heart rate, stroke volume, or both -amount of blood going to brain remains relatively the same always, however, more blodo would go to skeletal muscle instead of the abdomen
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blood velocity
the rate at which blood is moving through out blood vessels not constant; changes in different regions blood moves fast in arteries and arterioles, very slow through capillaries, and speeds up again in venules and veins
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relationship between blood velocity and area of vessels
velocity is inversely related to the cross sectional area of the vessels -capillaries have the greatest cross sectional area so blood passes through very slowly-- increases efficiency of gaseous exchange
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how is velocity manipulated
blood velocity can be manipulated locally by changing the diameter of the arterioles -if we dilate the arterioles, more blood goes through and travels faster -if we constrict the arterioles, less blood goes through an it travels
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metabolic mechanism for regulating blood flow
low levels of oxygen or nutrients cause vasodilation, as well as relaxation of the pre-capillary sphincter so that blood will flow through them and more blood is delivered to that area
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myogenic mechanism for regulating blood flow
blood vessels respond to the stretch that is exerted on their walls the more stretch, the more the vessel wants to push back, so it contracts when blood pressure is high in a certain area, the blood vessel dilates and diverts is to go somewhere else
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angiogenic mechanism for regulating blood flow
production of new blood vessels happens with people who train aerobically because more energy needs to go to the muscles this is a training adaptation
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respiratory gases and lipid soluble molecules pass across the walls of blood vessels through...
simple diffusion
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water soluble solutes pass through walls of blood vessels through...
intercellular clefts and fenestrations
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larger molecules pass through walls of blood vessels through...
caveoli
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fluids pass through walls of blood vessels through...
pinocytic vesicles through exocytosis or endocytosis
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capillary fluid dynamics
fluid is forced out through clefts at the arterial end of the capillary bed -this movement is regulated by balance between hydrostatic pressure and colloid osmotic pressure what is moved out at the arterial end comes back in the venous end
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hydrostatic pressure (fluid pressure)
the force exerted by a fluid against the thing that contains it hydrostatic pressure in the capillaries IS blood pressure capillary hydrostatic pressure is HIGHER on the arterial end, and LOWERS on the venous end due to loss of fluids (why fluid comes back in on venule end)
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colloid osmotic pressure
force created by non-diffusible components (mostly plasma proteins) the pressure of the blood wants to force fluid out, buy the proteins in the blood want fluid to come back in via osmosis (water moves toward the more concentrated side) **functions in opposition to hydrostatic pressure**
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four opposing forces that regulate movements in and out of the capillaries
1. capillary hydrostatic -- pushing out 2. interstitial hydrostatic -- pushing in 3. capillary colloid osmotic-- in blood, plasma proteins pull in 4. interstitial colloid osmotic
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most important force that regulates movement in/out of capillaries
capillary hydrostatic pressure
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net filtration pressure
results from the interaction between hydrostatic and colloid osmotic pressures determines if there is a net gain or loss of fluid from the capillaries
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portal systems
specialized capillary beds that exist between veins to the increase the amount of blood that we have serves regional tissue needs
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most important portal system
hepatic portal system (liver) this is needed because the liver has MANY important jobs
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hypovolemic shock
low blood volume due to bleeding that causes low blood pressure
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vascular shock
blood vessels are extremely dilated and causes low blood pressure
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cardiogenic shock
due to a failure of the heart pump the heart is damaged and can no longer contract (MI)
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embryological development of the vessels
composed of simple squamous epithelium heart lining continues tgrough the vessels Mesodermal orgigin 1. mesodermal cells collect in isolated pockets called blood islands and they are distributed throughout the embryo 2. the blood islands connect to form vascular tubes and secrete platelet derived growth factor. This signals mesenchymal cells to form muscular and fibrous coats
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atherosclerosis
deposits of plaque (usually cholesterol) that accumulate on the walls of the vessels -they reduce the size of the vessels, which reduces the space for blood flow
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who is less likely to suffer from atherosclerosis
females are less likely then men -estrogen helps break down cholesterol so plaque deposits don't build up
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hypertension
long-term high blood pressure -tiny vessels in brain can open (stroke) -capillaries can burst in eyes (blindness) -heart attacks -kidney disease -heart failure -sexual dysfunction