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145 Cards in this Set

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blood
liquid connective tissue
Plasma (key proteins)
Albumin- most common
Globulin-important for immune system
Fibrogen-critical for blood clotting
Hematocrit
Hemato-blood
crit-to judge
Judger of the blood
Viscosity
Measure how thick/thin your blood is
other components in blood
Nutrients (vitamins, mineral, energy sources)
Dissolved gasses
Waste products
Electrolytes (Na+)
Osmolarity
(105-106)
a measure of the amount of dissolved particles in a given volume of liquid
Water moves from regions of low osmolarity to high osmolarity.
Edema
outcome of not having enough osmolarity in the blood.
high BP
outcome of having a high osmolarity in the blood (low osmolarity in the tissue)
Table salt
High intake INCREASES osmolarity of the blood, resulting in water entry in to the blood.
Erythrocyte
(RBC) important for carrying Co2
Most common of all formed elements of the blood
Leukocyte
(WBC) comes in variety of forms
Platelets
not cells, cell fragments
Erythropoiesis
Formation of erythrocytes
Key proteins in the life of RBC
Kidney, liver; signaling centers via erythropotetin
bone marrow-birthplace (from stem cells)
Liver, spleen-graveyard
Your diet-iron,B vitamins.
Hypoxemia
fig 18.7
Low oxygen in blood, sensed and erythropoetin (promotes erythropoesis)
made by liver and kidney
Anemia
Lack of RBC, dont have enough hemoglobin. Caused by low iron heavy bleeding
Polycythemia
elevated levels of RBC, seen on people who go to high elevation because of lack of oxygen, production of RBC increases.
Sickle cell
genetically based mutation that alters the hemoglobin molecule causing a change in the shape of the cell. these cells get caught together and clump. can momentarily block off circulation of tissue (painful)
Thalassemia
Body doesn't make enough hemoglobin
Hemoglobin
Inside the RBC that causes the oxygen, its level indicates how well your blood causes oxygen processes the iron that supports the production of RBC.
RBC
Determines Blood type
Impacts transfusion
Blood typing
p.693 table 18.6
Agglutination
When an antibody bids to an antigen
anitbody
bind to antigens and
mark the cells bearing them for destruction
antigen
Glycolipids and glycoproteins on the erythrocyte surface determine your ABO and Rh blood groups, and function
as antigens
(WBC) Leukopoiesis
produces WBC
Stem Cells
in bone marrow, cells that have the ability to live throughout your lifespan and can replenish themselves. problems become apparent when there are problems with stemcells.
Origin of WBC
bone marrow, lymphatic tissue
(5 types of WBC)
Granulocytes
has granules
basophilis-obscure nucleus
Eosinophilis-visible nucleus
has 2 lobes
Neutrophilis-visible nucleus has 3 lobes
(5 types of WBC)
Basophilis
obscure nucleus
(5 types of WBC)
Eosinophilis
visible nucleus
has 2 lobes
(5 types of WBC)
neutrophilis
visible neucles
has 3 lobes
5 types of WBC
Granulocytes
Basophilis
eosinophilis
Neutrophilis
Agranulocytes
Monocytes-pleimorphic nucleus large cell size
Lympnocytes- round nucleus. small cell size
Leukemia
Cancer of the blood, damage to stem cells in bone marrow
Leukopenia
defencey in WBC
Leukocytosis
Elevated WBC can be elevated by allergies.
Immnosupression
granular cytoplasm
immune system will not work right
Bilirubin
Pigmented bile
made from the heme (iron)
part of hemoglobin, bile is produced by the liver
Jaundice-too much bilirubin
Thrombopoiesis
platelet formation
fxn: participant in and regulator of homeostasis; defense
origin: fragments of bone marrow cells
How blood clots form (3 steps)
1. vascular spasm vasoconstriction(vessel is closing) platlets release factors that help stimulate the muscle contraction
2.platelet blood formation-platelets aggregate and form a a plug to slow blood loss, collagen fibers act as a place for platelets to grab onto.
3. Coagulation: takes the longest but is the longest lasting. blood clot is formed designed to effectively seal off the wound so there is no excess blood loss. Fibrin (protein) makes blood clot.
Fibrin
found as inactive precursor called fibrinogen, signals to form a clot from platelet and injured tissue converts fibrinogen to fibrin
Intrinsic factors
Things in the blood that operate independent of other influences. their build into blood this is why you can take blood out of the body and put it into the test tube and it will clot by itself.
Extrinsic Mechanism
relies on signals outside of the blood like the damaged tissues or blood vessels.
Hemophilia
Genetic condition where people have a deficiency in blood clotting factors. person tends to belled easily rely on blood transfusions.
Thrombocytopenia
lower than normas (reduced) level of platlets
Thrombosis
people prone to blood clots . clots from in veins, if blood clot breaks loose, it travels down towards the lungs, if it gets lodged in the lungs...
DIC
Disseminated Intravascular Coagulation
Widespread thorough the body. problem s clots cut off blood supply to important organs, killing the organs, then the person. KIC is found alot in peopl ewith sepsis (pathoens in blood causing disease) people with sepsis take anticoagulants to reduce blood clots
Sepsis
Pathogens in blood causing. people with sepsis take anticoagulants to reduce blood clots.
Embolism
traveling blood clot, life threatening can cut off blood to vital part of the body.
Using enzymes to produce universal RBC
the challenge : shortage of RBC avaiable for transfuson. only 7% of blood donors in USA are O-
Solution : convert type A,AB, and B blood to type O blood
how: use enzymes to remove the A and B antigens from erythrocytes.
Circuit
pathway of blood flow
Pulmonary circuit
goes to the lungs
Systematic circuit
goes everywhere else
Arteries
takes blood AWAY from the heart
takes blood...
Veins
takes blood TO the heart
takes blood...
Right side of heart
sends blood to the lungs
sends blood ....
Left side of heart
receiving blood from the lungs
receives blood...
Inbalance
too much blood in one spot
get an overload of blood excess blood causes fluid to accumulate in lungs. congestion heart failure.
Heart
found in teh pericardial cavity
four chambered, one way directional set up
Pericardial cavity
contains fluid
contains...
periteal pericardium
the sac that encloses the heart and cavity
sac
Pericardium fluid
acts as lubrication, makes sure the heart doesnt rub against the pericardium
lubrication
outer wall
in contact with the fluid
contact
Flow of blood
through the cavities inside of the heart
cavities
endocardium
Innermost layer that comes in contact with the blood
innermost
Myocardium
muscle of the heart (myo) the working layer of the heart. controls the pumping. part that suffers most with oxygen deprivation. when damaged it scared and replaced with scar tissue which doesn't work as well.
muscle
Valves of the heart
Atrioventricular valves (AV
Tricuspid valve
Bicuspid valve
AV
TRI
BI
Tricuspid valve
between the right atrium and ventricle
right
Bicuspid valve
between left atrium and ventricle
pressure on the atrium opens the valve, pressure on the ventricle side encloses the valve
myocardium is thicker on the ventricle than the atrium, there are tendons connected (tendionous cords) to the bi and tricuspid valve which limits their movements so blood cant flow in the other direction.
Valve prolapse
some people have damage to this system where the cords don't do their job, so the valves push and the pressure builds up in the ventricle. valve doesn't seal and wont keep blood from blowing backwards (regurgitation of the blood)
regurgitation
Heart Murmur
way to know-listen to your heart
can develop or be genetic
Semilunar valves
Right- aorta valve (goes from body to lungs)
Left- Pulmonary valve (goes from lungs to body
Reason blood flows
Pressure is lower on one side of the valve than the other (tends to gravitate towards lower pressure)
Reason pressure changes
Has to do with the ventricles are actually contracting . If they are contracting, pressure goes up, if they are relaxing, pressure goes down.
V<A
if ventricle is relaxed the blood collects in the right artery.
V>A
If ventricles contract it pushes blood close tot eh AV valves causing blood to migrate to the side with less pressure.
Cardiac muscle:
Pacemaker
Electrical activity that initiates the heart itself (influenced by nerves)
conduction system
some cardiac cells don't contract but instead generate action potentials (electrical impulses)
intercalated discs
cardiac muscle cells are electrically connected by these.
allows atria to contract in unison and the ventricles to contract together (although separately)
Steps of conductivity:
Sinoatrial node (pacemaker)
(1)
Located in the right atrium.
spontaneously discharges
most peoples heart rate is 60-70
more efficient on a slower rate
HR is governed by the pacemaker.
Right and Left Atrium
(2)
stimulated to contract. blood is going to get pushed through the ventricle
Atrioventricular Node
(3)
often called the "gateway to the ventricle"
from this point on it is heading sraight way for all the vntricles. takes time for blood to ill teh ventricles.
slowest step due to ventricles needing to be filled with blood. after this step process speeds up dramatically
Atrioventricaular bundle
(4)
Dead center of the heart. sends messages to the bundle branches.
Bundle branches
(5)
go further to the purkinje fibers
Purkinje fibers
(6)
spread throughout the entire heart allowing the heart to be able to contract.
Right and left ventricles
(7)
the process is completed.
the blood ends up here.
Ventricular fibrillation
Sometimes instead of gaining info from step 1, for some reason the heart develops other signals. led by numerous conduction, mixed messages.
end up "fiddling"
Uncontrolled fiddling of the heart.
Flutters
increase contraction doesn't allow the chamber to fill. not productive in moving blood.
Defibrillaton
Restoring the heart to a neat and orderly fashion.
attaches patches to the heart, hopefully allowing the heart to recover and beat properly.
Blocks
Heart damaged
the signal for electrical travel cant get through. it has a physical block, such as scar tissue. just sits there waiting
install pacemaker to clear blocks.
Electrocardiogram
visualizing the hearts electrical activity
Heartbeat
ripples of electro-activity that come and go
Depolarization
triggers a change in membrane cell
Re-polarization
restoring it back to its initial state, in which it is ready for another stimulus.
when can contraction start?
when the ventricles are filled with blood
for every depolarization there is a...
re-polarization
Bicuspid valve opening initiates...
Ventricular filling
Atrial contraction
completes ventricular filling
Heart sound S1
corresponds with isovolumetric CONTRACTION and the start of ventricular contraction and opening of aortic valve
Heart sound S2
corresponds with isovolumetric RELAXATION when the bicuspid and aortic valves are both closed
ventricular output
should be equal to keep both circuits in balance
lower red line
atrium
upper red line
aorta
Black line
ventricle- dramatic changes in pressure
Diastolic
relaxation in ventricle
Systolic
contraction in the ventricle
atrial emptying
starts before the atrial contractions
what does squeezing do?
raises pressure rapidly in the left ventricle, as the pressure goes up its higher in the atrium closing the bicuspid valve.
isovolumetric contraction
fraction of time when both valves are closed.
blood volume doesn't change during this period.
causes the first heart sound S1
Cardiac output
determines the amount of blood that leaves the heart. heart rat x stroke volume
Factors that accelerate the heart rate
sympathetic cardiac nerves (calcium deficiency)
Factors that decelerate the heart rate
Parasympathetic vagus nerves (calcium excess)
Vagus nerves
Revieve info from the medulla of the brain (has the cardiac center on it) communicates to the heart, to the SA and AV nodes.
Body has the ability to demand the heart rate depending on your activity
slow the heart
things that can change the HR
Body position
blood pressure
chemical nature on the blood (blood gasses)
Electrolytes
Calcium levels- if out of range, def speed up, excessive slow heart
Potassium- severe diarrhea results with loss of Ka+
Tachycardia
Increased HR
Bradycardia
Decreased HR
Cardiac nerves
accelerate the heart (compare to vagus nerves)
moderate the fxn of nerves
a person with tachycardia, need to stimulate the vagus nerve so its more active trying to slow down teh heart.
Stroke volume
preload
frank-starling law of the heart
contractiblity
afterload
myocardial infraction
periostin
Preload
blood volume presented int eh ventricles volume effects before contraction. (the more blood entering the heart, the more blod leaving the heart)
Frank-Starling law of the heart
Stroke volume is proportional to tend- diastolic volume.
Ventriular output is adjusted relative to volume of blood entering the heart. this helps balance the output of the two sides of the heart. (howmuch blood that is allowed to enter the heart is going to govern how much blood can leave the heart) if ventricle is gaining extra, the heart adapts to the extra blood will be ejected. if one side of the heart is ejected more blood, that more blood will return to the other side of the heart, and stroke volue will increase.
Inbalance- can over load the body or lungs.
Contractibility
how strong the contraction is- inotropic agents.
if myocardium is weak contraction will be weak.
Medication to balance out.
the stronger teh contraction teh more blood is pumped out
afterload
pressure opposing exit of blood from heart. vessels the blood is going to enter once the blood is pumped out of the ventricles.
Resistance- pressure opposing the exit of blood from the heart.
Afterload: pressure in the pulminary trunk
if there is pressure in the PT and aorta it will reduce cardiac output, problem with hypertension. because the amt of blood leaving the heart is decreased., the heart has to work harder to push out blood.
Myocardial infarction
whatever tissue is effected gets replaced by scar tissue. this tissure stretches the things out because of the pressure inside of the ventricle pushes it out.
a solution
promote cardiac repair via periostin
periostin
a chemical that awakens the regenerative nature of our heart.
most cells in our body are
4-6 width from the nearest blood vessel
there are about 60,000 miles of blood vessels contained in our body
3 classes of vessels
arterial vessels
capillary
veins
arterial vessels
carry blood away from the heart (the diameter of teh vessel gets narrower as you get farther from the heart) get smaller as they move away rom teh heart. do not have valves (ensure one way blood flow) uch more elastic than veins
capillary
has the thinest wall, 1 cell layer, exchange vessels, designed for the exchange of substances moving in and out of the blood.
veins
carry blood toward the heart. get larger as they move toward teh heart. have valves (ensure one way blood flow. not very elastic
elastic lamina
present in teh arteries elasticity for the arteries
tunicia exterina
outer most layer of teh artery, anchors teh vessel to the tissur
tuncia media
thickest layer
middle
is a muscle (has to be able to contract ) strenght layer of teh vessel
vasomotion
atrtery dilates and enlarges
aneurysm
wall weakness. when the wall develops a weakness due to damage of infection, maybe high BP having a stressed part of the bdoy, weakenign teh wall. typically a problem in the arterial end of things. the wall could ru[ture causing ta hole can lead to hemorrhaging. if it doesnt buldge it coud be building upressure on a part of the body that isnt used to pressure.
atherosclerosis
stiff arteries
conducting artery
can dilate/constrict.
lessens fluctuations in BP
less stress on downstream vessles
arteiole
smallest artery
Vena cava
large gein
venule
smallest vein
vessels
the vessels as they operate have and elastic nature to them which can control blood flow to various parts of teh body.
also dampens teh stress on the vessels with the blod being pumped out of the heart into the vessels
if you have stiff arteries, it will not allow the vessels to expand tna let teh blood into the vessels.
can cause damage to teh vessel.
another cause for aneurysm
vasomotion
constriction and relaxation int eh vessel (vessel opens and closes) runing legs need vessel dilate to teh legs.